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Efficacy of automatic multimodal device therapy for ventricular tachyarrhythmias as delivered by a new implantable pacing cardioverter-defibrillator. Results of a European multicenter study of 102 implants.

BACKGROUND: Third-generation implantable cardioverter-defibrillators are devices designed to treat ventricular tachycardia (VT) and ventricular fibrillation (VF) by means of overdrive pacing, cardioversion, or defibrillation. So far, the efficacy of tiered therapy has been documented only in small series. Therefore, a European multicenter clinical evaluation study of a new tachyarrhythmia control device, the Medtronic PCD pacer-cardioverter-defibrillator with epicardial patch-lead configuration, was undertaken. METHODS AND RESULTS: We report on 102 patients (mean age, 55 +/- 13 years) from 11 European centers. PCD devices implanted between May 1989 and February 1991 were included. The patients suffered from hemodynamically significant ventricular tachyarrhythmias not suppressed by antiarrhythmic drug therapy and unrelated to acute myocardial infarction; one patient had nonsustained VT and severely depressed left ventricular function. Seventy patients had coronary artery disease with old myocardial infarctions, 23 had cardiomyopathies of various etiologies, and nine patients had no detectable heart disease. Mean ejection fraction was 36 +/- 14% (range, 10-76%). Mean intraoperative defibrillation threshold (51 patients) was 10.6 +/- 5.1 J (range, 2-18 J). The documented follow-up ranged from 1 to 21 months (mean, 9.4 +/- 5.8 months), or 79.9 cumulative patient-years. Perioperative mortality was 3.9%. The actuarial survival rate at 12 months was 91%. One sudden arrhythmic death occurred. Sixty patients (58%) received device therapy. Seventeen patients had therapies only for "VF" episodes, 16 patients only for VT, and 28 patients for VT and "VF" episodes. Based on device memory data, 1,235 spontaneous VT episodes were detected and treated in 43 patients. Twelve hundred four of these VT episodes received painless initial antitachycardia pacing therapy, restoring sinus rhythm in 91%. The 108 ongoing episodes received 209 multiple therapeutic attempts. Eighty-five additional overdrive pacing therapies restored sinus rhythm in 30%. Initial ineffective antitachycardia pacing therapies received 51 cardioversion pulses. The success rate was 61%. Seventy-three additional cardioversion pulses were delivered to backup ineffective pacing therapy as well as ineffective secondary cardioversion pulses. Their success rate was only 40%. Two hundred eighty-six spontaneous episodes were detected in 44 patients as "VF." Overall defibrillation efficacy was 97.6%. CONCLUSIONS: The implanted device nearly eliminates sudden arrhythmic death in patients with documented, potentially fatal ventricular tachyarrhythmias. Automatic tiered therapy is highly effective to restore sinus rhythm, provided that an integrated two-zone tachycardia detection algorithm is used, assigning lower tachycardia rates to overdrive pacing and/or cardioversion and higher tachycardia rates to defibrillation. In general, spontaneous VTs can be terminated by automatic overdrive pacing, and painful or disturbing countershock therapies are not required to terminate the majority of spontaneous VT episodes.

Death, Sudden, Cardiac↗

Large change in voltage at phase reversal improves biphasic defibrillation thresholds. Parallel-series mode switching.

BACKGROUND: Multiple factors contribute to an improved defibrillation threshold of biphasic shocks. The leading-edge voltage of the second phase may be an important factor in reducing the defibrillation threshold. METHODS AND RESULTS: We tested two experimental biphasic waveforms with large voltage changes at phase reversal. The phase 2 leading-edge voltage was twice the phase 1 trailing-edge voltage. This large voltage change was achieved by switching two capacitors from parallel to series mode at phase reversal. Two capacitors were tested (60/15 microfarads [microF] and 90/22.5 microF) and compared with two control biphasic waveforms for which the phase 1 trailing-edge voltage equaled the phase 2 leading-edge voltage. The control waveforms were incorporated into clinical (135/135 microF) or investigational devices (90/90 microF). Defibrillation threshold parameters were evaluated in eight anesthetized pigs by use of a nonthoracotomy transvenous lead to a can electrode system. The stored energy at the defibrillation threshold (ion joules) was 8.2 +/- 1.5 for 60/15 microF (P < .01 versus 135/135 microF and 90/90 microF), 8.8 +/- 2.4 for 90/22.5 microF (P < .01 versus 135/135 microF and 90/90 microF), 12.5 +/- 3.4 for 135/135 microF, and 12.6 +/- 2.6 for 90/90 microF. CONCLUSIONS: The biphasic waveform with large voltage changes at phase reversal caused by parallel-series mode switching appeared to improve the ventricular defibrillation threshold in a pig model compared with a currently available biphasic waveform. The 60/15-microF capacitor performed as well as the 90/ 22.5-microF capacitor in the experimental waveform. Thus, smaller capacitors may allow reduction in device size without sacrificing defibrillation threshold energy requirements.

Animals↗

Potential cost-effectiveness of public access defibrillation in the United States.

BACKGROUND: Approximately 360,000 Americans experience sudden cardiac arrest each year; current treatments are expensive and not very effective. Public access defibrillation (PAD) is a novel treatment for out-of-hospital sudden cardiac arrest that refers to use of automated external defibrillators by the lay public or by nonmedical personnel such as police. A clinical trial has been proposed to evaluate the effectiveness of public access defibrillation, but it is unclear whether such early defibrillation will offer sufficient value for money. Our objective was to estimate the potential cost-effectiveness of public access defibrillation by use of decision analysis. METHODS AND RESULTS: A decision model compared the potential cost-effectiveness of standard emergency medical services (EMS) systems with that of EMS supplemented by PAD. We considered defibrillation by lay responders or police, using an analysis with a US health-care perspective. Input data were derived from published data or fiscal databases. Future costs and effects were discounted at 3%. Monte Carlo simulation was performed to estimate the variability in the costs and effects of each program. Sensitivity analyses assessed the robustness of the results to changes in input data. A standard EMS system had a median cost of $5900 per cardiac arrest patient (interquartile range, IQR, $3200 to $10,900) and yielded a median of 0.25 quality-adjusted life years (IQR, 0.20 to 0.30). PAD by lay responders had a median incremental cost of $44,000 per additional quality-adjusted life year (IQR, $29,000 to $68,900). PAD by police had a median incremental cost of $27,200 per additional quality-adjusted life year (IQR, $15,700 to $47,800). The results were sensitive to changes in the cost and relative survival benefit of PAD. CONCLUSIONS: Although more expensive than standard EMS for sudden cardiac arrest, PAD may be economically attractive. The effectiveness and cost-effectiveness of PAD should be assessed in a randomized, controlled trial.

Cost-Benefit Analysis↗

Influence of phase duration of biphasic waveforms on defibrillation energy requirements with a 70-microF capacitance.

BACKGROUND: Phase duration of biphasic shocks may be an important determinant of defibrillation success. The purpose of this study was to investigate the effect of changing phase duration of biphasic pulses delivered by 70-microF capacitors on defibrillation energy requirements. This may be clinically relevant for the optimization of implantable cardioverter-defibrillator design and programming. METHODS AND RESULTS: Defibrillation thresholds (DFTs) were determined for 13 waveforms in 13 pigs by application of a 70-microF capacitance and a transvenous/submuscular lead system. In part I, phase-1 duration varied, preserving a phase-1/phase-2 duration ratio of 60%/40%. The phase-1 durations were 1, 2, 3, 4, 5, and 6 ms. The DFT was lowest (22.9+/-7 J) for phase 1=3 ms compared with phase 1=1 ms (36.4+/-7.5 J), 2 ms (25+/-6.5 J), 4 ms (25+/-7.6 J), 5 ms (30.7+/-7.3 J), or 6 ms (32.9+/-8.1 J) (P<.001). In part II, phase-1 duration was 3 ms but phase-2 duration varied: 0.7, 1.3, 2, 2.7, 3.3, 4, and 6 ms. Significant DFT minima were found at phase 2=2 ms (22.5+/-4.2 J) and phase 2=4 ms (22.5+/-4.2 J) compared with phase 2=0.7 ms (31.7+/-9.3 J), phase 2=3.3 ms (26.7+/-6.1 J), or phase 2=6 ms (28.3+/-6.8 J) (P<.05). CONCLUSIONS: The strength-duration curve of biphasic defibrillation shocks demonstrates a single optimum for phase-1 duration. In contrast, two optima with minimal energy requirements were found for phase-2 duration. Optimization of both phases of low-capacitance biphasic shocks may reduce energy requirements for defibrillation.

Animals↗

Improved internal defibrillation success with shocks timed to the morphology electrogram.

BACKGROUND: A previous retrospective study by our group suggested that shocks timed to the upslope of the shocking lead electrogram improved defibrillation efficacy. The goal of this study was to prospectively determine whether defibrillation threshold could be reduced by use of an algorithm that timed shocks to the upslope of coarse ventricular fibrillation (test treatment) compared with shocks delivered asynchronously after 10 seconds of fibrillation (control treatment). METHODS AND RESULTS: Ten pigs were instrumented with a 3-lead system for internal defibrillation. Initial estimates of the energy required to achieve defibrillation E50 for both treatments were made by an up/down method. Subsequently, additional shocks at V50+/-10% and V50-20% were given for each treatment to obtain data points at higher and lower intensities. Probability-of-success curves were estimated for both treatments by the best-fit method. Energies required were significantly lower for the timed shocks than for the asynchronous shocks (P<0.00 1). E80 was reduced 15.5%, from 27.1+/-2.5 to 22.9+/-1.8 J (P<0.002). The width of the probability-of-success curve (E80-E20) for the test treatment was also significantly narrower than that for the control treatment (7.1+/-0.9 versus 10.8+/-1.7, P<0.01). Normalized curve width (E80-E20)/E50 was decreased from 51+/-5% of E50 for control shocks to 37+/-4% of E50 for synchronous shocks (P<0.02). CONCLUSIONS: In this model, defibrillation threshold is lower and more deterministic when shocks are timed to the upslope of the shocking lead electrogram. If a similar reduction is observed in humans, shock timing may lower defibrillation threshold and simplify programming of shock intensity.

Algorithms↗

Increasing fibrillation duration enhances relative asymmetrical biphasic versus monophasic defibrillator waveform efficacy.

Biphasic waveforms reduce defibrillation threshold compared with corresponding monophasic waveforms. However, effects of fibrillation duration on relative efficacy of monophasic and biphasic waveforms are unknown. This study used a newly developed defibrillation model, the isolated right- and left-sided working rabbit heart, with epicardial defibrillation electrodes, to compare threshold for a monophasic waveform (5 msec rectangular) and an asymmetrical biphasic waveform (5 msec each pulse, V2 = 50% V1). Mean voltage defibrillation threshold (V50) was determined from sigmoidal probability of successful defibrillation versus shock intensity curves after 5, 15, and 30 seconds of fibrillation in a paired study with 10 hearts. Results showed that biphasic waveforms had significantly lower voltage and energy thresholds at all fibrillation durations and that their relative efficacy improved with increasing fibrillation duration. Biphasic voltage threshold was 38.2 +/- 2.2, 44.7 +/- 4.8, and 46.6 +/- 3.2 V after 5, 15, and 30 seconds of fibrillation compared with monophasic thresholds of 51.7 +/- 4.4 (p less than 0.002), 63.0 +/- 7.6 (p less than 0.05), and 72.1 +/- 3.9 V (p less than 0.005). Biphasic waveform energy threshold was 0.67 that for the monophasic waveform after 5 seconds of fibrillation (0.12 +/- 0.01 versus 0.18 +/- 0.03 J, p less than 0.05). The ratio between biphasic waveform threshold and monophasic waveform threshold (B/M) decreased to 0.62 at 15 seconds. At 30 seconds, B/M was 0.52 (0.17 +/- 0.02 versus 0.33 +/- 0.04 J, p less than 0.02). This study also showed that biphasic waveform threshold was a nonlinear function of monophasic waveform threshold so that improved biphasic defibrillator waveform efficacy was greatest for hearts having higher monophasic thresholds.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Epicardial mapping of ventricular defibrillation with monophasic and biphasic shocks in dogs.

To study the mechanism of defibrillation and the reason for the increased defibrillation efficacy of biphasic waveforms, the potential gradient in a 32 x 30-mm region of the right ventricle in 15 dogs was progressively lowered in four steps while a strong potential gradient field was maintained throughout the rest of the ventricular myocardium. The volume of right ventricle beneath the plaque was 10 +/- 2% of the total ventricular mass. A 10-msec monophasic (eight dogs) or 5/5-msec biphasic (seven dogs) truncated exponential shock 30% above the defibrillation threshold voltage was given via electrodes on the left ventricular apex and right atrium to create the strong potential gradient field. Simultaneously, a weaker shock with the same waveform but opposite polarity was given via mesh electrodes on either side of the small right ventricular region to cancel part of the potential difference in the region and to create one of the four levels of potential gradient fields. Shock potentials and activations were recorded from 117 epicardial electrodes in the small region, and in one dog global epicardial activations and potentials were recorded from a sock containing 72 electrodes. Each gradient field was tested 10 times for successful defibrillation after 10 seconds of electrically induced fibrillation. For both monophasic and biphasic shocks, the percentage of successful defibrillation attempts decreased (p < 0.05) as the potential gradient decreased in the small region. Defibrillation was successful approximately 80% of the time for a mean +/- SD potential gradient of 5.4 +/- 0.8 V/cm for monophasic shocks and 2.7 +/- 0.3 V/cm for biphasic shocks (p < 0.05). No postshock activation fronts arose from the small region for eight waveform when the gradient was more than 5 V/cm. For both waveforms, the postshock activation fronts after the shocks were markedly different from those just before the shock and exhibited either a focal origin or unidirectional conduction.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Virtual electrode-induced phase singularity: a basic mechanism of defibrillation failure.

Delivery of a strong electric shock to the heart remains the only effective therapy against ventricular fibrillation. Despite significant improvements in implantable cardioverter defibrillator (ICD) therapy, the fundamental mechanisms of defibrillation remain poorly understood. We have recently demonstrated that a monophasic defibrillation shock produces a highly nonuniform epicardial polarization pattern, referred to as a virtual electrode pattern (VEP). The VEP consists of large adjacent areas of strong positive and negative polarization. We sought to determine whether the VEP may be responsible for defibrillation failure by creating dispersion of postshock repolarization and reentry. Truncated exponential biphasic and monophasic shocks were delivered from a bipolar ICD lead in Langendorff-perfused rabbit hearts. Epicardial electrical activity was mapped during and after defibrillation shocks and shocks applied at the plateau phase of a normal action potential produced by ventricular pacing. A high-resolution fluorescence mapping system with 256 recording sites and a voltage-sensitive dye were used. Biphasic shocks with a weak second phase (<20% leading-edge voltage of the second phase with respect to the leading-edge voltage of the first phase) produced VEPs similar to monophasic shocks. Biphasic shocks with a strong second phase (>70%) produced VEPs of reversed polarity. Both of these waveforms resulted in extra beats and arrhythmias. However, biphasic waveforms with intermediate second-phase voltages (20% to 70% of first-phase voltage) produced no VEP, because of an asymmetric reversal of the first-phase polarization. Therefore, there was no substrate for postshock dispersion of repolarization. Shocks producing strong VEPs resulted in postshock reentrant arrhythmias via a mechanism of phase singularity. Points of phase singularity were created by the shock in the intersection of areas of positive, negative, and no polarization, which were set by the shock to excited, excitable, and refractory states, respectively. Shock-induced VEPs may reinduce arrhythmias via a phase-singularity mechanism. Strong shocks may overcome the preshock electrical activity and create phase singularities, regardless of the preshock phase distribution. Optimal defibrillation waveforms did not produce VEPs because of an asymmetric effect of phase reversal on membrane polarization.

Animals↗

Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles.

BACKGROUND: The role of intracellular calcium (Ca(i)) in defibrillation and vulnerability is unclear. METHODS AND RESULTS: We simultaneously mapped epicardial membrane potential and Ca(i) during shock on T-wave episodes (n=104) and attempted defibrillation episodes (n=173) in 17 Langendorff-perfused rabbit ventricles. Unsuccessful and type B successful defibrillation shocks were followed by heterogeneous distribution of Ca(i), including regions of low Ca(i) surrounded by elevated Ca(i) ("Ca(i) sinkholes") 31+/-12 ms after shock. The first postshock activation then originated from the Ca(i) sinkhole 53+/-14 ms after the shock. No sinkholes were present in type A successful defibrillation. A Ca(i) sinkhole also was present 39+/-32 ms after a shock on T that induced ventricular fibrillation, followed 22+/-15 ms later by propagated wave fronts that arose from the same site. This wave propagated to form a spiral wave and initiated ventricular fibrillation. Thapsigargin and ryanodine significantly decreased the upper limit of vulnerability and defibrillation threshold. We studied an additional 7 rabbits after left ventricular endocardial cryoablation, resulting in a thin layer of surviving epicardium. Ca(i) sinkholes occurred 31+/-12 ms after the shock, followed in 19+/-7 ms by first postshock activation in 63 episodes of unsuccessful defibrillation. At the Ca(i) sinkhole, the rise of Ca(i) preceded the rise of epicardial membrane potential in 5 episodes. CONCLUSIONS: There is a heterogeneous postshock distribution of Ca(i). The first postshock activation always occurs from a Ca(i) sinkhole. The Ca(i) prefluorescence at the first postshock early site suggests that reverse excitation-contraction coupling might be responsible for the initiation of postshock activations that lead to ventricular fibrillation.

Action Potentials↗

Defibrillation--a burning issue in coronary care units!

Skin burns are accepted to be a complication of defibrillation, however there is no published data on their frequency, cause and treatment. A postal questionnaire survey was designed to assess the relative frequency of defibrillation burns in coronary care units and identify the possible factors contributing to their occurrence. Treatments prescribed in coronary care units were also noted. The questionnaire was sent to the Senior Sister/Charge Nurse in all 263 coronary care units in the United Kingdom. 232 Replies were received (88.2%). Defibrillation burns were seen in 98.7% of CCU's. Ten contributory factors were proposed. The commonest implicated cause was recurrent defibrillation. The most frequently prescribed topical treatment was 1% silver sulphadiazine cream (Flamazine). Defibrillation burns are relatively common in coronary care units. Many result from recurrent defibrillation and may be unavoidable in the patient undergoing prolonged resuscitation. However there are other identifiable factors which, if avoided, may lead to a reduction in the number of burns seen.

Burns↗

Intracardiac voltage gradients during transthoracic defibrillation: implications for postshock myocardial injury.

UNLABELLED: In-vitro studies indicate that the electric-field intensity, or voltage gradient (VG), generated by a defibrillation shock is a determinant of defibrillation success as well as potential shock-induced cardiac injury. It is not clear how common descriptors of shock dose, e.g., joules (J), relate to VGs. OBJECTIVES: To assess the relationships between shock energy descriptors and VG. METHODS: One monophasic and three biphasic waveforms were compared using transthoracic shocks and standard electrodes in five swine. VG measurements via intracavitary multielectrode-tipped catheters were compared with delivered energy and peak current. Shock variables were recorded at native transthoracic impedance and an adjusted impedance approximating that of typical humans. RESULTS: For shocks at the same energy setting, peak current and VGs varied widely among the four defibrillators. At simulated human impedance (75 Omega), shocks at each device's maximum energy setting produced similar VGs among the three biphasic defibrillators, despite different delivered energies. For both native impedance (35 Omega) and at 75 Omega, VG correlated with peak current (r = 0.81 and 0.77, respectively) but not energy setting (r = 0.61, 0.52) or delivered energy (r = 0.58, 0.56). At the maximum energy setting of each device, maximum recorded VGs for both monophasic (33 V/cm) and biphasic (24 V/cm) defibrillators were less than those reported to cause myocardial injury (>60 to 80 V/cm). CONCLUSIONS: Energy descriptors correlate poorly to actual shock intensities. When compared with reported VG thresholds of myocardial injury, this study suggests that risk of injury from critically strong VGs is low for all of these defibrillators and equivalent among tested biphasic waveforms.

Animals↗

The effects of cardioversion and defibrillation on left ventricular systolic function.

The purpose of this research was to evaluate the left ventricular systolic function behavior after cardioversion and defibrillation. The study included 18 adult patients who had direct current cardioversion or defibrillation performed for conversion of spontaneous or induced arrhythmias. All patients were submitted to a careful medical evaluation and an M-mode echocardiogram before cardioversion or defibrillation. The clinical and echocardiographic evaluations were repeated immediately after, and 6 and 12 h following the countershock. Six hours after cardioversion or defibrillation a statistically significant (p = .04) decrease in contractility (circumferential fiber shortening and ejection fraction) was observed without significant changes in preload (end diastolic volume), heart rate or afterload (end systolic stress and diastolic arterial pressure). Within 12 h, the left ventricular systolic dysfunction disappeared. The impairment of systolic function was independent of the amount of energy used, the type of arrhythmia, the rhythm after cardioversion or defibrillation and the etiologic cardiac diagnoses. There was a significant (p = .03) direct, negative and linear correlation between left ventricular systolic indices (ejection fraction and circumferential fiber shortening) before the countershock and the amount of decrease in systolic function after the countershock. In spite of the fact that most patients had a low ejection fraction, none of them presented clinical signs of heart failure. Defibrillation and cardioversion produce a transient decrease in cardiac contractility which is independent of the amount of energy used and does not produce clinical signs of heart failure.

Arrhythmias, Cardiac↗

Ethmozine and ethacizine--new antiarrhythmic drugs with defibrillating properties.

Ventricular fibrillation (VF) is a life-threatening arrhythmia that leads to death unless electrical defibrillation is applied in time. Recent publications indicate that VF can be either sustained (SVF), requiring electrical defibrillation, or transient (TVF), reverting spontaneously into sinus rhythm. Since VF cannot be totally prevented by drugs, a new antiarrhythmic therapeutic approach has been proposed: drug-induced enhancement of the ability of the heart to defibrillate by itself. In this study we examined the defibrillating potency of two antiarrhythmic phenothiazines, ethmozine (ETM) and ethacizine (ETA), as well as their effects on catecholamine uptake and on the electrophysiological properties of the myocardial cell membrane. The antiarrhythmic-defibrillatory activity was examined in cats; the inhibitory effect on [3H]-norepinephrine (NE) uptake was examined in rat brain synaptosomes, and the electrophysiological membrane effects were examined by microelectrode recordings in perfused strips of heart ventricle from guinea-pigs. The results indicate that: 1. ETA exhibits similar but stronger antiarrhythmic-defibrillating and NE reuptake inhibitory effects than ETM; 2. ETA at 10-6 M decreases ventricular conduction time and increases Vmax while ETM at this concentration does not change them; 3. The defibrillating ability of the drugs can be related to their inhibitory potency on NE reuptake. We suggest that the risk of sympathomimetic arrhythmogenicity is prevented by the previously described, membrane stabilizing Class 1 antiarrhythmic properties of these drugs.

Action Potentials↗

Automated external defibrillators: technical considerations and clinical promise.

Early defibrillation is the most important determinant of survival for victims of cardiac arrest due to ventricular fibrillation. The automated external defibrillator (AED) was developed as the result of the American Heart Association's Public Access Defibrillation initiative. The goal of this initiative is to place AEDs in strategic locations so that laypersons with minimal training could promptly defibrillate victims of cardiac arrest. Because of changes in design and the use of alternative waveforms for defibrillation, the modern AED is compact and portable, simple to use, and highly efficacious; in addition, it requires little maintenance. Automated external defibrillators have been used successfully by traditional and nontraditional responders as well as laypersons. In special environments, such as casinos and commercial aircraft, AEDs have performed particularly well. State and federal legislation has eased concerns about AED use by extending legal protection to AED users under Good Samaritan laws. Since the experience continues to be positive, AEDs are being used in increasingly diverse community locations, and public awareness is growing. The American Heart Association's initiative is progressing rapidly.

Aircraft↗

How to launch a community early defibrillation program.

More than 60 emergency services professionals attended an EMS Today 2001 preconference symposium, "How to Champion Public Access Defibrillation in Your Community: Leadership, Art and Science," hosted by AED manufacturer Philips/Heartstream. Their goal: to learn the practicalities of starting and maintaining an early defibrillation program in their communities. The recent increase in research and attention to community early defibrillation programs led Philips/Heartstream to host the symposium, which featured cardiac arrest survivor Diane Jackson, as well as three community early defibrillation program advocates who've implemented early defibrillation programs in their communities. Their advice for kick-starting early defibrillation programs in your community follows.

Cooperative Behavior↗

[Acute cardiovascular failure and its treatment--value of defibrillation in preclinical management].

Ventricular fibrillation is the most common cause of cardiac arrest. The only scientifically proved therapy that guarantees a long time survival is the early electrical defibrillation. As early as 200 years ago electricity was employed in trying to regain circulation in cases of unexpected death. In the field of emergency medicine almost all rescue services are equipped with defibrillators nowadays and the personnel is trained in using them. Since the application of electricity on the myocardium can lead to damage, there are devices with a varied defibrillation pulse available since recently. The advantage of the biphasic defibrillation is a less harmful impact on the myocardium at lower shock intensity. A further novelty which enables the application by groups other than the rescue services, is the automatic external defibrillator (AED). Extending the availability of defibrillators can contribute to an increase in the presently low success rates of resuscitation.

Algorithms↗

[Early defibrillation in the treatment of sudden cardiac arrest].

Recovery from nontraumatic cardiac arrest depends on the presence of all the elements in the chain of survival. "Early defibrillation" is critical because ventricular fibrillation is the most common initial dysrhythmia of sudden cardiac arrest. Defibrillation is the only treatment, and survival from ventricular fibrillation is determined by time. Out-of-hospital studies have demonstrated that defibrillation provided by first responders improves survival. Technologic advances have simplified defibrillation delivery through the development of automated external defibrillators (AEDs). Early defibrillation programs with AEDs are quickly becoming a standard of care for emergency medical service systems throughout the United States. Improvement in in-hospital survival rates from cardiac arrest is not as evident as in the emergency medical service community. Medical centers need to assess response times to cardiac arrest and implement AED programs. All the nurses should learn to use an AED as part of basic life support training.

Clinical Competence↗

Electrophysiological concept of ventricular defibrillation mechanism.

Sudden cardiac death is a major health problem in most industrialized countries around the world including Thailand. It is mainly caused by ventricular fibrillation (VF). Currently, defibrillation is the only effective clinical treatment of this fatal arrhythmia. Although defibrillation mechanism has been investigated extensively for many decades, its definite mechanism is still debated. It is known that understanding the basic mechanism of defibrillation is essential to develop better treatment of VF: In the present article, seven hypotheses commonly proposed as the mechanism of ventricular defibrillation are reviewed. Since research in the field of defibrillation mechanism is dynamic, the present review is to update the information to clinicians and basic investigators on the mechanism of defibrillation available to date.

Electric Countershock↗