(Circulation. 2000;101:2968.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
Resuscitation After Prolonged Ventricular Fibrillation With Use of Monophasic and Biphasic Waveform Pulses for External Defibrillation
From the Division of Cardiology (C.T.L., H.C., R.D.B., H.R.H.), Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Md; the Department of Emergency Medicine (N.A.P.), Putnam Memorial Hospital, Bennington, Vt; and the Department of Biomedical Engineering (A.C.L., K.R., H.R.H.), Johns Hopkins University, Baltimore, Md.
Correspondence to Charles T. Leng, MD, The Johns Hopkins Hospital, Carnegie 568, 600 N Wolfe St, Baltimore, MD 21287. E-mail cleng{at}mail.jhmi.edu
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Abstract |
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Background—Survival after prolonged ventricular fibrillation (VF) appears severely limited by 2 major factors: (1) low defibrillation success rates and (2) persistent post-countershock myocardial dysfunction. Biphasic (BP) waveforms may prove capable of favorably modifying these limitations. However, they have not been rigorously tested against monophasic (MP) waveforms in clinical models of external defibrillation, particularly where rescue from prolonged VF is the general rule.
Methods and Results—We randomized 26 dogs to external countershocks with either MP or BP waveforms. Hemodynamics were assessed after shocks applied during sinus rhythm, after brief VF (>10 seconds), and after resuscitation from prolonged VF (>10 minutes). Short-term differences in percent change in left ventricular +dP/dtmax (MP -16±28%, BP +9.1±24%; P=0.03) and left ventricular -dP/dtmax (MP -37±26%, BP -18±20%; P=0.05) were present after rescue from brief VF, with BP animals exhibiting less countershock-induced dysfunction. After prolonged VF, the BP group had lower mean defibrillation thresholds (107±57 versus 172±88 J for MP, P=0.04) and significantly shorter resuscitation times (397±73.7 versus 488±74.3 seconds for MP, P=0.03).
Conclusions—External defibrillation is more efficacious with BP countershocks than with MP countershocks. The lower defibrillation thresholds and shorter resuscitation times associated with BP waveform defibrillation may improve survival after prolonged VF arrest.
Key Words: ventricular fibrillation • defibrillation waveform • resuscitation
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Introduction |
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Much of our experience with biphasic (BP) waveform defibrillation stems from its widespread use in implantable cardioverter-defibrillators. In the setting of brief-duration ventricular fibrillation (VF), BP waveform pulses have demonstrated significantly lower defibrillation thresholds (DFTs) than standard monophasic (MP) waveform pulses.1 2 3 However, they have not been tested extensively in prehospital models of external defibrillation for which prolonged cardiac arrest and severe myocardial stunning are often overriding considerations.
Time-dependent increases in DFTs have been well described for MP waveforms4 and for BP waveforms after relatively brief durations of VF.5 Little is known, however, about the energy requirements for BP defibrillation after prolonged arrest. BP waveforms may rescue victims who might otherwise have failed defibrillation with conventional MP waveforms. In addition, the lower energy BP countershocks may produce less myocardial injury and mechanical dysfunction than equally effective MP countershocks.
The present study tested the hypothesis that BP waveforms are more efficacious than MP waveform countershocks in an animal model of out-of-hospital VF arrest. The primary aim was to test for differences in DFTs and overall resuscitation outcomes between the 2 waveforms. Secondary aims were to characterize the effects of countershocks on myocardial function and to clarify the importance of coronary perfusion pressures before defibrillation on resuscitation outcomes after prolonged cardiac arrest.
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Methods |
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All experiments were conducted in accordance with the "Position of the American Heart Association on Research Animal Use" and with the approval of the Animal Care and Use Committee at The Johns Hopkins University.
Animal Preparation
Twenty-six consecutive mongrel dogs (25 to 28 kg) were studied.
Anesthesia was induced with intravenous sodium
thiopental (12.5 to 15.0 mg/kg) before endotracheal intubation and
maintained with 1% to 3% isoflurane delivered with an
anesthesia ventilator (Narkomed, North American
Dräger). ECG leads were placed for continuous monitoring. Millar
micromanometer catheters (7F) were placed through
femoral sheaths and positioned in the right atrium (RA) and ascending
aorta under fluoroscopic guidance. An 8F
micromanometer pigtail catheter was similarly
placed in the left ventricle (LV), and a pacing catheter was placed in
the right ventricular apex. Adhesive defibrillation
electrodes (Ballard) were applied to the left and right thorax, with
the left-sided electrode as the anode for the MP pulse and the first
phase of the BP pulse. Arterial blood gases were monitored,
and ventilator adjustments were made to achieve an arterial
PCO2 between 35 and 45 mm Hg
and pH between 7.35 and 7.45. An infusion of lactated Ringer’s
solution was regulated to maintain an LV end-diastolic
pressure of 8 to 12 mm Hg.
Equipment
A custom defibrillator with a capacitor size of 100 µF was
used to generate a BP truncated exponential waveform with fixed phase 1
and phase 2 pulse durations of 6 and 4 milliseconds, respectively. A
standard defibrillator was used to deliver a critically damped
sinusoidal MP waveform. These test waveforms are illustrated in Figure 1
. Chest compressions were performed with
a vest CPR system previously developed in our laboratory.6
The thoracic vest was inflated and deflated at 60 cycles per minute
with peak vest pressures set between 225 and 235 mm Hg.
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Experimental Protocols
Animals were randomized to either MP or BP countershocks.
Initial assessments of baseline hemodynamics were
followed by stacked countershocks administered (1) during sinus rhythm,
(2) after 10 seconds of VF, and (3) after 10 minutes of unsupported VF.
These protocols were performed in the same sequence in all animals as
described below. Step-up energy protocols were devised to reach maximum
device outputs within 5 steps. The MP sequence was 50, 100, 200, 300,
and 360 J; the BP sequence was 50, 70, 120, 150, and 170 J.
Synchronous Countershocks
Transthoracic countershocks were administered at
30-second intervals during sinus rhythm by using the randomized
waveform and step-up sequence. Hemodynamics were
recorded during the protocol and for 15 minutes after the final
countershock.
Brief VF
Fibrillation was induced through the right
ventricular pacing wire with 60-Hz alternating current.
Unsynchronized countershocks were initiated after 10 seconds of VF by
using the assigned waveform and step-up sequence until VF was
terminated. The energy level of the first successful countershock was
designated as the DFT. Hemodynamics were sampled
immediately before and after VF, as well as 15 minutes after successful
defibrillation.
Protracted VF
The animals were reinduced into VF, and general
anesthesia was discontinued on establishment of VF. After
10 minutes of unsupported VF, 3 interventions were serially performed
until a perfusing rhythm was restored: (1) an immediate attempt at
defibrillation, (2) vest CPR at 11 minutes, followed by a second
round of defibrillation at 15 minutes if necessary, and (3)
epinephrine (1 mg IV) at 16 minutes, followed by a third round
of defibrillation at 19 minutes if necessary (see Figure 2).
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Stacked countershocks were delivered until successful defibrillation or maximum device outputs were achieved. Rescue crossovers to the alternate waveform with use of a single maximum energy countershock were allowed after 19 minutes of refractory VF and for recurrent fibrillation events. All VF recurrences were terminated with prompt countershocks, starting with the last effective energy and waveform.
CPR was halted on return of spontaneous circulation (ROSC). Epinephrine (1 mg IV) boluses were administered every 5 minutes if required to maintain LV systolic blood pressure (LVSBP) >50 mm Hg. At 40 minutes, all animals were dosed with a final epinephrine bolus regardless of hemodynamic stability and observed during a 10-minute washout period. Surviving animals were euthanized at 50 minutes. Necropsy was limited to animals without ROSC.
Definitions
Defibrillation was defined as the maintenance of a
rhythm other than VF for a minimum of 30 seconds. ROSC required a
perfusing rhythm capable of supporting LVSBP >50 mm Hg for at
least 1 minute. Study deaths were prospectively defined as the
following: (1) >19 minutes of uninterrupted VF, (2) rescue crossover
to the alternate waveform, and (3) no return of spontaneous circulation
(NROSC). Study survivors were categorized as capable of self-sustaining
blood pressure (SSBP) or nonsustaining blood pressure (NSBP) on the
basis of their ability or inability to support LVSBP>50 mm Hg
during a period of epinephrine washout.
Data Analysis/Calculations
An oscillograph (Gould) was used to record RA, aortic, and
LV pressures. The maximal rates of the rise and fall of LV pressure
(ie, +dP/dtmax and
-dP/dtmax) were determined by differentiation of
LV pressures. Coronary perfusion pressure (CPP) was calculated
as the instantaneous difference between end-diastolic
aortic and RA pressures. The time difference between successful
defibrillation and onset of ROSC was designated as the post-arrhythmic
mechanical arrest interval.
Statistics
Sample size was calculated to detect a 40-J difference in DFTs
after prolonged VF; a SD of 50, a power of 80%, and P=0.05
were assumed. Continuous and categorical variables were evaluated
with the unpaired t test (2-tailed) and
2 analysis, respectively. Repeated
measures ANOVA was used to test for variance in LV contractile function
and loading conditions; then paired t tests (2-tailed) were
performed to isolate differences for our prospective end points. All
results were reported as mean±SD. A value of P=0.05 was
considered significant.
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Results |
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Baseline Characteristics
Baseline LV hemodynamics and loading conditions were not different between the 2 randomized groups. In addition, clinical resuscitation factors did not differ significantly between groups (Table 1
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Defibrillation Efficacy
Mean DFTs were consistently lower for the BP waveform than
for the MP waveform (Figure 3).
Increasing the duration of VF had the effect of raising DFTs for both
waveforms. After 10 seconds of VF, there was a strong trend
(P=0.07) toward lower mean DFTs for the BP waveform (56±26
versus 109±93 J for MP). After 10 minutes of VF, there was a
significantly lower DFT for the BP waveform (107±57 versus 172±88 J
for MP, P=0.04).
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All defibrillation attempts were successful after brief VF; however, defibrillation failures occurred after prolonged VF. Notably, 3 of 13 MP animals failed countershocks to 360 J but were successfully rescued with a single BP countershock at 170 J. In contrast, only 1 of 13 BP animals failed countershocks to 170 J but proved refractory to MP rescue countershocks at 360 J. This animal represented the only death attributable to refractory VF in the present study and was excluded from calculations of mean DFT.
Countershock-Induced Myocardial Dysfunction
Greater hemodynamic impairment was
consistently observed in the MP group, with larger initial
drops in dP/dtmax and less complete recovery
after countershocks than in the BP group (Figure 4). Percent change versus baseline
suggested significant intergroup differences in
+dP/dtmax (MP -16±28%, BP +9.1±24%;
P=0.03) and -dP/dtmax (MP -37±26%,
BP -18±20%; P=0.05) after termination of brief VF, with
more pronounced effects on -dP/dtmax than on
+dP/dtmax for both waveforms.
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0.05.LV loading conditions were serially assessed during each phase of the experimental protocol. No significant differences in RA pressure, heart rate, LVSBP, and LV end-diastolic pressure were appreciated at baseline, after synchronized countershocks, or after brief VF (repeated measures ANOVA, F=0.29; P=NS).
Resuscitation Outcomes After Prolonged Arrest
Although 19 of 26 animals were defibrillated within the first
round of stacked countershocks, 6 remained in VF until a subsequent
round of defibrillation. Rhythms after defibrillation were pulseless
electrical activity in 19 animals, asystole in 4, and sinus rhythm in
2. Refractory VF was observed in 1 animal.
Significant differences in resuscitation times were noted between
randomized groups (Figure 5). Mean ROSC
occurred at 488±74.3 and 397±73.7 seconds for MP and BP animals,
respectively (P=0.03). This was associated with longer
periods of contractile arrest after successful MP countershocks, with
postarrhythmic mechanical arrest intervals of 429±86 seconds for the
MP group versus 271±168 seconds for the BP group (P=0.02).
In 1 MP animal, supervening VF interrupted ROSC and delayed
resuscitation substantially (ROSC time 1254 seconds). This MP outlier
was excluded to provide the most conservative estimate of group
differences.
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Supervening VF
interrupted ROSC in a single MP outlier (ROSC time 1254 seconds) that
was excluded to more conservatively estimate group differences.
Study death occurred in 7 of 13 MP animals (Table 2): 4 remained pulseless (NROSC), 1
required BP rescue but remained pulseless after defibrillation
(crossover death), and 2 were resuscitated only after BP rescue
(crossover death/ROSC). In contrast, only 3 of 13 BP animals were study
deaths: 1 remained pulseless (NROSC), 1 exhibited refractory VF, and 1
remained pulseless because of a catheter-based hemorrhage
confirmed on necropsy. A strong trend toward reduced mortality in the
BP group was demonstrated by use of intention-to-treat analysis
(2 2.6, P<0.11). The difference
reached statistical significance, however, when the fatal complication
was excluded (2 3.7, P=0.05).
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Post-Resuscitation Myocardial Dysfunction
Although more BP animals were resuscitated, the percentage of
animals exhibiting SSBP in the BP group (5 of 10) and the MP group (3
of 6) was not different. More quantitative statements could not be made
regarding relative degrees of postresuscitation myocardial dysfunction,
because steady-state measurements could not be established in animals
that were often dependent on inotropic support and subject to
variable postresuscitation loading conditions.
Subgroup analysis was performed on the 6 animals that initially
failed defibrillation (Table 3). Despite
longer mean arrest intervals (immediate defibrillation 615±13 seconds,
delayed defibrillation 1152±270 seconds; P=0.002), ROSC
occurred in 5 of 6 animals. All 3 BP animals had SSBP, 2 MP crossover
death animals had NSBP, and 1 MP crossover death animal had NROSC. A
longer mean ROSC time in the delayed defibrillation group was not
significant, having been offset by a marked decrease in the mean
postarrhythmic mechanical arrest interval (immediate defibrillation
409±67 seconds, delayed defibrillation 72±93 seconds;
P=0.0002). Interestingly, the only 2 animals to be
defibrillated directly into perfusing rhythms were BP animals in this
delayed defibrillation subgroup.
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Discussion |
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To the best of our knowledge, the present study is the first to describe the following: (1) lower biphasic DFTs after 10 minutes of unsupported VF, (2) milder degrees of countershock-induced contractile dysfunction with biphasic pulses, and (3) shorter postarrhythmic mechanical arrest intervals resulting in earlier resuscitation after biphasic defibrillation. These findings suggest that certain BP waveforms may have a significant impact on resuscitation from prolonged VF and that their continued development in external defibrillators will result in improved survival.
Defibrillation Efficacy of MP and BP Waveforms
Lower BP waveform DFTs have been reported versus MP waveforms for
internal defibrillation of brief VF.1 2 3 Available
evidence suggests that BP pulses are similarly efficacious in external
defibrillators.7 8 Although our data demonstrated only a
strong trend toward lower BP energy requirements after brief VF
(P=0.07), our lowest energy countershock (50 J) likely
exceeded the actual DFT recently reported in a similar experimental
model (20.3±4.4 J).8
DFTs and first-shock efficacy rates have been reported as superior for BP waveforms despite increasing VF durations. However, arrest intervals have seldom been >30 seconds.2 4 9 Walcott et al8 recently reported the external DFTs of MP and BP waveforms after 15 seconds of VF and then 3 minutes of unsupported VF. They reported a 2-fold increase in mean DFTs over time for the MP waveform but no increase in mean DFTs for the BP waveform. Our BP data, however, documented significant increases in DFTs after 10 seconds and then 10 minutes of unsupported VF (56±26 and 107±57 J, respectively; P=0.02). Nevertheless, the available data suggest that certain BP waveforms are less susceptible to time-dependent increases in DFTs than are MP waveforms.
External DFTs proved significantly lower for the BP group than the MP group despite >10 minutes of VF. No other studies have compared DFTs under such extreme conditions of global ischemia after prolonged arrest. Furthermore, 3 of 4 arrhythmic deaths that failed multiple defibrillation attempts with their assigned waveform were salvaged after crossover to the BP waveform. The remaining arrhythmic death failed to defibrillate with either waveform. Collectively, this suggests that lower energy BP countershocks may prove capable of rescuing sudden-death victims who might otherwise have failed defibrillation with conventional MP devices.
Countershock-Induced Contractile Dysfunction
Although there is growing evidence that countershocks can induce
myocardial injury,10 11 12 the extent to which they
contribute to contractile dysfunction independently of VF and global
ischemia remains unclear. Several lines of evidence support the
hypothesis that countershocks at clinically relevant current dosages
are harmful to myocardium. Transient ECG changes
consistent with myocyte damage have been reported after
transthoracic countershocks12 and appear to be
corroborated by the release of myocardium-specific
enzymes13 and ultrastructural damage to cardiac
myocytes.10 These indirect markers of countershock-induced
injury, however, have proven difficult to correlate with surprisingly
variable effects on myocardial function.
Studies using MP waveforms have demonstrated either no effect14 15 or relatively minor effects16 17 18 on contractile function after brief cycles of fibrillation and defibrillation. Contractile abnormalities were originally described by Kerber et al,16 who used repeated high-energy epicardial countershocks and implantable subepicardial sonomicrometers in an open-chest dog model. Subsequent work in a dog model of epicardial defibrillation17 and in human subjects undergoing transthoracic defibrillation18 revealed inconsistent effects on systolic function but significant impairments in diastolic function. Waveform characteristics, current dosage, and lead configuration varied significantly between studies. Furthermore, the impact of pericardotomy on myocardial function and the relative sensitivities of various noninvasive methods for detecting subtle functional impairments were difficult to assess. Differences in experimental design may be responsible for perceived inconsistencies in the study literature.
Previous work comparing MP with BP waveforms has largely ignored postcountershock sequelae. However, significantly less ST-segment elevation has been reported after transthoracic defibrillation with BP waveforms than with MP waveforms of equal efficacy.12 Similarly, less harmful effects on mitochondrial function and oxidative metabolism have been documented after epicardial defibrillation with BP countershocks than after energy-matched MP countershocks.19 In spite of these findings, differential effects on actual myocardial function by particular electrical waveforms have not previously been described.19 20
Countershocks delivered in sinus rhythm had inconsequential effects on myocardial function; however, significant effects were apparent after countershock termination of brief VF. In the present study, BP defibrillation resulted in less severe functional consequences than did MP defibrillation. Diastolic function was more impaired than systolic function for both waveform types, with more prominent filling impairments after MP countershocks persisting for up to 15 minutes. A self-limited decrease in systolic function after MP defibrillation and an unexpected increase in systolic function after BP defibrillation were also noted. Because these transient effects on systolic performance were seldom present for >1 to 2 minutes, we speculated that differential effects on adrenergic tone might be contributory.15 18 21 Although it is not entirely clear whether these effects were the result of an interaction between arrhythmia and waveform or carryover effects from repeated countershocks, the potential impact of defibrillatory waveforms could not be dismissed. The present study provides compelling evidence that transthoracic countershocks may exert unintended effects upon contractile function and that the choice of defibrillation waveform may have important clinical consequences on myocardial function.
Effect of Defibrillation Waveform on Resuscitation Outcomes After
Prolonged Arrest
Perhaps our most intriguing study finding is that BP countershocks
significantly reduced overall resuscitation times. After prolonged VF,
a difference of >90 seconds in mean resuscitation time was evident
between randomized groups. Quicker resuscitation could only in small
part be attributed to more efficient defibrillation and trivially
shorter delays in charging lower energy BP capacitors. Improvements
were largely due to shorter periods of contractile arrest after
successful BP countershocks. This observation suggests a clear
advantage of BP over MP countershocks in the treatment of VF arrest,
for which differences of seconds to minutes often prove critical to
recovery.
Jones and Jones22 described significantly shorter durations of contractile arrest after electrical field stimulation with BP pulses in a cell culture model of defibrillation. Exposure to equivalent energy MP pulses resulted in longer contractile arrest intervals on photocell mechanogram tracings and prolongation of myocyte depolarization.23 These investigators suggested that intrinsic properties of the MP waveform predisposed to membrane electroporation and that subsequent derangements of ion homeostasis were responsible for diminished cellular excitability and contractile arrest. These studies loosely corroborate our in vivo work with intact fibrillating hearts and support our contention that lower energy BP countershocks exert less harmful effects on excitation-contraction coupling. Furthermore, our results suggest that direct effects of electrical waveforms are not simply masked by the myocardial depressant effects of prolonged fibrillation and ischemia but appear fully capable of potentiating post-resuscitation myocardial dysfunction.
More efficient defibrillation and prompter hemodynamic recovery translated predictably into fewer BP study deaths after prolonged VF. The relatively few BP deaths (3 of 13 animals) included the only animal that proved refractory to defibrillation with either waveform, as well as the only fatal technical complication encountered in the study. No such extenuating circumstances were noted among the MP deaths (7 of 13 animals). Consideration of longer-term end points and neurological death would likely have favored additional survival benefits for the BP group.
Postresuscitation Myocardial Stunning After Prolonged
Arrest
Postresuscitation myocardial stunning is generally thought to be
mediated by global no-flow myocardial ischemia. However,
experimental work using isolated-perfused hearts induced into VF
suggests that the electrochemical activity of the arrhythmia
itself may, in the absence of ischemia, contribute to
excitation-contraction uncoupling via intracellular calcium
overload.24 Electrical countershocks may potentiate this
effect and have furthermore been linked to the dose-dependent release
of free radicals25 and to waveform-specific effects on
mitochondrial function and oxidative
metabolism.19 Therefore, it seems reasonable
to speculate that high-energy MP countershocks might contribute to more
profound myocardial stunning through one of the above mechanisms.
A spectrum of progressive myocardial stunning was assumed in our experimental model. Resuscitated animals capable of SSBP were considered less severely stunned than animals with NSBP. However, the present study lacked sufficient power to detect a significant difference with the use of such crude qualitative assessments of stunning severity. Furthermore, the greater number of study deaths in the MP group likely resulted in significant statistical censoring.
Predefibrillation CPR After Prolonged Arrest
Prompt restoration of CPP has long been considered critical to the
success of resuscitation from VF.26 Whether immediate
defibrillation is always the best strategy remains controversial. Work
by Niemann et al27 suggests that pretreatment with CPR and
epinephrine before defibrillation will improve resuscitation
after prolonged arrest. It remains unclear, however, whether the study
effect was due to an order dependence of treatment or to differences in
epinephrine utilization.
Delays to defibrillation were encountered in 6 animals that failed immediate defibrillation. Subgroup analysis suggested favorable outcomes for this cohort despite significantly longer arrest intervals. Our delayed defibrillation subgroup exhibited a surprising trend toward overall improved resuscitation rates and less severe myocardial dysfunction versus the immediate defibrillation subgroup despite comparable CPP during CPR. These data suggest that CPR prior to BP defibrillation may prove to be a superior resuscitation strategy for prolonged VF arrest and that countershock waveforms are indeed capable of modifying the course of postresuscitation myocardial dysfunction.
Study Limitations
We prospectively chose to standardize peak vest pressures rather
than clamp measured CPP during chest compressions. As a result, there
was a nonsignificant difference in CPP after randomization. Lack of
rigorous control of ventricular loading conditions
presented another limitation. Because much of the data resulted
from paired comparisons both before and after electrical countershocks,
it seems reasonable to assume that loading conditions did not change
appreciably except for very transient effects immediately after shock
administration. Finally, the present study was neither capable of
elucidating the underlying mechanisms of improved BP defibrillation
efficacy nor of assessing the relative contributions of
ischemia, VF, electrical waveform, or cumulative current dosage
on post-arrest myocardial function.
Clinical Implications
BP waveforms may prove more effective than standard MP
waveform countershocks in rescuing patients with out-of-hospital VF
arrest. They may prove to have an impact on immediate arrest survival
by (1) rescuing patients who might otherwise have failed defibrillation
with standard MP pulses, (2) minimizing post-countershock myocardial
dysfunction, and (3) reducing overall resuscitation times. Perhaps
the most significant improvements in overall arrest survival will be
attributable to the evolution of smaller, less expensive, and more
widely available automated external BP defibrillators.
Received April 27, 1999; revision received January 11, 2000; accepted January 31, 2000.
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  P. J. Kudenchuk, L. A. Cobb, M. K. Copass, M. Olsufka, C. Maynard, and G. Nichol Transthoracic Incremental Monophasic Versus Biphasic Defibrillation by Emergency Responders (TIMBER): A Randomized Comparison of Monophasic With Biphasic Waveform Ascending Energy Defibrillation for the Resuscitation of Out-of-Hospital Cardiac Arrest due to Ventricular Fibrillation Circulation, November 7, 2006; 114(19): 2010 - 2018. [Abstract] [Full Text] [PDF]
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G. Manoharan, N. Evans, D. Allen, J. Anderson, and J. Adgey Comparing the Efficacy and Safety of a Novel Monophasic Waveform Delivered by the Passive Implantable Atrial Defibrillator With Biphasic Waveforms in Cardioversion of Atrial Fibrillation Circulation, April 6, 2004; 109(13): 1686 - 1692. [Abstract] [Full Text] [PDF]
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J. T. Niemann, D. Garner, E. Khaleeli, and R. J. Lewis Milrinone Facilitates Resuscitation From Cardiac Arrest and Attenuates Postresuscitation Myocardial Dysfunction Circulation, December 16, 2003; 108(24): 3031 - 3035. [Abstract] [Full Text] [PDF]
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R.A. Samson, R.A. Berg, R. Bingham, D. Biarent, A. Coovadia, M.F. Hazinski, R.W. Hickey, V. Nadkarni, G. Nichol, J. Tibballs, et al. Use of Automated External Defibrillators for Children: An Update: An Advisory Statement From the Pediatric Advanced Life Support Task Force, International Liaison Committee on Resuscitation Circulation, July 1, 2003; 107(25): 3250 - 3255. [Full Text] [PDF]
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C. T. Leng, R. D. Berger, H. Calkins, A. C. Lardo, N. A. Paradis, and H. R. Halperin Electrical Induction of Ventricular Fibrillation for Resuscitation From Postcountershock Pulseless and Asystolic Cardiac Arrests Circulation, August 7, 2001; 104(6): 723 - 728. [Abstract] [Full Text] [PDF]
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