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Left atrial chamber and appendage function after internal atrial defibrillation: a prospective and serial transesophageal echocardiographic study.

OBJECTIVES: The purpose of this prospective study was to assess left atrial chamber and appendage function after internal atrial defibrillation of atrial fibrillation and to evaluate the time course of recovery. BACKGROUND: External cardioversion of atrial fibrillation may result in left atrial appendage dysfunction ("stunning") and may promote thrombus formation. In contrast to external cardioversion, internal atrial defibrillation utilizes lower energies; however, it is unknown whether the use of lower energies may avoid stunning of the left atrial appendage. METHODS: Transesophageal and transthoracic echocardiography were performed in 20 patients 24 h before and 1 and 7 days after internal atrial defibrillation to assess both left atrial chamber and appendage function. Transthoracic echocardiography was again performed 28 days after internal atrial defibrillation to assess left atrial function. The incidence and degree of spontaneous echo contrast accumulation (range 1+ to 4+) was noted, and peak emptying velocities of the left atrial appendage were measured before and after internal atrial defibrillation. To determine left atrial mechanical function, peak A wave velocities were obtained from transmitral flow velocity profiles. RESULTS: Sinus rhythm was restored in all patients. The mean +/- SD peak A wave velocities increased gradually after cardioversion, from 0.47 +/- 0.16 m/s at 24 h to 0.61 +/- 0.13 m/s after 7 days (p < 0.05) and 0.63 +/- 0.13 m/s after 4 weeks. Peak emptying velocities of the left atrial appendage were 0.37 +/- 0.16 m/s before internal atrial defibrillation, decreased significantly after internal atrial defibrillation to 0.23 +/- 0.1 m/s at 24 h (p < 0.01) and then recovered to 0.49 +/- 0.23 m/s (p < 0.01) after 7 days. The corresponding values for the degree of spontaneous echo contrast were 1.2 +/- 1.2 before internal atrial defibrillation versus 2.0 +/- 1.0 (p < 0.01) and 1.1 +/- 1.3 (p < 0.01) 1 and 7 days after cardioversion, respectively. One patient developed a new thrombus in the left atrial appendage, and another had a thromboembolic event after internal atrial defibrillation. CONCLUSIONS: Internal atrial defibrillation causes depressed left atrial chamber and appendage function and may result in the subacute accumulation of spontaneous echo contrast and development of new thrombi after cardioversion. These findings have important clinical implications for anticoagulation therapy before and after low energy internal atrial defibrillation in patients with atrial fibrillation.

Anticoagulants↗

Clinical shock tolerability and effect of different right atrial electrode locations on efficacy of low energy human transvenous atrial defibrillation using an implantable lead system.

OBJECTIVES: The objectives of this study were 1) to evaluate the effect of different right atrial electrode locations on the efficacy of low energy transvenous defibrillation with an implantable lead system; and 2) to qualitate and quantify the discomfort from atrial defibrillation shocks delivered by a clinically relevant method. BACKGROUND: Biatrial shocks result in the lowest thresholds for transvenous atrial defibrillation, but the optimal right atrial and coronary sinus electrode locations for defibrillation efficacy in humans have not been defined. METHODS: Twenty-eight patients (17 men, 11 women) with chronic atrial fibrillation (AF) (lasting > or = 1 month) were studied. Transvenous atrial defibrillation was performed by delivering R wave-synchronized biphasic shocks with incremental shock levels (from 180 to 400 V in steps of 40 V). Different electrode location combinations were used and tested randomly: the anterolateral, inferomedial right atrium or high right atrial appendage to the distal coronary sinus. Defibrillation thresholds were defined in duplicate by using the step-up protocol. Pain perception of shock delivery was assessed by using a purpose-designed questionnaire; sedation was given when the shock level was unacceptable (tolerability threshold). RESULTS: Sinus rhythm was restored in 26 of 28 patients by using at least one of the right atrial electrode locations tested. The conversion rate with the anterolateral right atrial location (21 [81%] of 26) was higher than that with the inferomedial right atrial location (8 [50%] of 16, p < 0.05) but similar to that with the high right atrial appendage location (16 [89%] of 18, p > 0.05). The mean defibrillation thresholds for the high right atrial appendage, anterolateral right atrium and inferomedial right atrium were all significantly different with respect to energy (3.9 +/- 1.8 J vs. 4.6 +/- 1.8 J vs. 6.0 +/- 1.7 J, respectively, p < 0.05) and voltage (317 +/- 77 V vs. 348 +/- 70 V vs. 396 +/- 66 V, respectively, p < 0.05). Patients tolerated a mean of 3.4 +/- 2 shocks with a tolerability threshold of 255 +/- 60 V, 2.5 +/- 1.3 J. CONCLUSIONS: Low energy transvenous defibrillation with an implantable defibrillation lead system is an effective treatment for AF. Most patients can tolerate two to three shocks, and, when the starting shock level (180 V) is close to the defibrillation threshold, they can tolerate on average a shock level of 260 V without sedation. Electrodes should be positioned in the distal coronary sinus and in the high right atrial appendage to achieve the lowest defibrillation threshold, although other locations may be suitable for certain patients.

Adult↗

[Analysis of ventricular fibrillation signals for the evaluation of defibrillation success in the treatment of ventricular fibrillation].

OBJECTIVE: Precise detection of ventricular fibrillation (VF), reliable prediction of defibrillation success and adjustment of the discharge waveform to the patient's transthoracic impedance may contribute to a reduction of electricity-associated myocardial injury caused by unnecessary counter shocks. Specifically, asystole thresholds distinguish between VF and asystole, and thus prevent unnecessary defibrillation attempts. We reviewed various studies and manufacturer characteristics regarding the parameters and algorithms for analyzing arrhythmia ECG signals. METHODS: Asystole threshold values of several defibrillator manufacturers were collected and a literature review was performed including the following parameters: amplitude, frequency, bispectral analysis, amplitude spectrum area, wavelets, nonlinear dynamics, N(alpha)histograms, and combinations of various parameters. RESULTS: The manufacturer dependent asystole thresholds vary substantially. We show ways to optimize an ECG-based analysis for the next technological generation of defibrillators. During advanced cardiac life support (ACLS) the probability of defibrillation success should be estimated. Optimal defibrillation waveform, depending on transthoracic resistance, should be individually determined. In case of prolonged VF with a low ECG amplitude defibrillation should not be attempted unless coronary perfusion has been improved by further measures of ACLS. The combined evaluation of VF amplitude and frequency is effective in predicting defibrillation success. Estimation of further parameters is potentially useful for guiding optimal timing of defibrillation. At present, the implementation of most parameters in out-of-hospital cardiopulmonary resuscitation (CPR) is limited by the lack of technical feasibility of online computing. CONCLUSION: Analysis of VF ECG signals should allow adequate VF detection as well as prediction of defibrillation success. Suitable asystole thresholds for analysis of ECG signals have to be determined, and the adverse effects of CPR associated artefacts on data analysis have to be reduced. Analysis of VF ECG signals is a precondition of individually optimized defibrillation and may contribute substantially to an increased quality of CPR.

Algorithms↗

Defibrillation energy requirements and electrical heterogeneity during total body hypothermia.

OBJECTIVE: Determine the effects of hypothermia on defibrillation energy requirements and cardiac electrophysiology. DESIGN: Prospective randomized acute intervention trial. SETTING: Medical center animal laboratory. SUBJECTS: Fifteen domestic farm swine. INTERVENTIONS: Swine were randomized to a hypothermia group (n = 8) or a control group (n = 7). All animals were instrumented with a transvenous defibrillation system connected to a defibrillator that delivers a biphasic-truncated waveform. Values for defibrillation energy requirements were measured at baseline (normothermia, 38-40 degrees C) and during treatment with total body hypothermia (30 degrees C) or no temperature change (sham). Hypothermia was induced by circulating ice-water through anterior and posterior surgical thermal blankets. MEASUREMENTS AND MAIN RESULTS: Defibrillation energy requirement values at 20%, 50%, and 80% were determined by using an up/down method. In the hypothermia group, defibrillation energy requirement values at baseline did not significantly change during hypothermia (defibrillation energy requirements 50% = 14 +/- 2 J vs. 15 +/- 2 J, respectively). Similarly, the defibrillation energy requirement values in the control group did not change from baseline to sham phase (defibrillation energy requirements 50% = 12 +/- 1 J vs. 13 +/- 1 J, respectively). Hypothermia profoundly affected cardiac electrophysiology, decreasing ventricular fibrillation threshold by 72%, conduction velocity by 25% (p < .01), and tissue excitability, while it prolonged ventricular repolarization and refractoriness by 7.5% to 15%, respectively (p < .05). CONCLUSIONS: Total body cooling to 30 degrees C was highly arrhythmogenic, although this unstable electrophysiological state did not alter ventricular defibrillation energy requirements. These data suggest that hypothermia may be used to slow metabolic processes without concern over the ability to successfully defibrillate and treat hypothermia-induced arrhythmias.

Animals↗

Effects of verapamil and Bay K 8644 on defibrillation energy requirements in dogs.

Antiarrhythmic drugs are often required in patients with implantable cardioverter-defibrillator devices. Prior evidence suggests that drugs modulate defibrillation energy requirements by altering ion channel activity. To evaluate the effects of calcium ion channel activity on internal defibrillation energy requirements, the calcium antagonist verapamil and Bay K 8644, a calcium channel activator, were investigated in 30 open-chest, pentobarbital-anesthetized dogs. Defibrillation energies were applied across two epicardial patch electrodes. The likelihood of successful defibrillation was determined at various shock energy levels, and the 50 and 90% effective energy doses were calculated using nonlinear regression. In saline control experiments (n = 10), the stability of the preparation throughout the 6-h duration of the experiments could be demonstrated. Verapamil administration (n = 10) infused to a mean plasma concentration of 69 ng/ml increased the 50 and 90% effective defibrillation energies by 41 and 43% (p less than 0.05), respectively, and to a mean plasma verapamil concentration of 170 ng/ml by 95 and 75% (p less than 0.01), respectively. The mean cycle length during ventricular fibrillation decreased with verapamil and was inversely related to the change in defibrillation energy requirement. Administration of Bay K 8644 (n = 10) produced a slight increase in the 50% effective defibrillation energy (25%; p less than 0.05) and 90% effective defibrillation energy (17%; n.s.). The electrophysiologic effects of verapamil were neither prevented nor reversed by Bay K 8644. In conclusion, intravenous verapamil administration caused an increase in defibrillation energy requirements, but the mechanism by which verapamil exerted this effect remains unclear. These experimental data suggest that verapamil should be used in patients with automatic implantable cardioverter-defibrillator devices only after individual testing.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

The effect of multiple shocks on canine cardiac defibrillation.

To determine if multiple shocks adversely affect the success of later shocks compared with early shocks, we analyzed the success rates of initial shocks (defibrillation attempts 1-5), first half shocks (defibrillation attempts 1-20) and second half shocks (defibrillation attempts 21-40) in a canine model. Epicardial patches were placed on the right and left ventricle in 28 dogs. Ventricular fibrillation was induced by a 60-Hz shock. After 30 seconds, defibrillation was attempted using 7, 12, 13, or 18 joules with either a uniphasic or biphasic rectangular waveform. The uniphasic waveform was 5 msec in duration; the biphasic waveform was 10 msec, with the lagging 5-msec pulse one-half the amplitude of the leading 5-msec pulse. For uniphasic shocks, the right ventricular patch was positive; for biphasic shocks, the right ventricular patch was positive during the leading 5 msec of the shock and negative during the lagging milliseconds. A total of 960 fibrillation episodes were evaluated; no dog was involved in more than 40 fibrillation episodes. The success rates of defibrillation attempts 1-5, defibrillation attempts 1-20, and defibrillation attempts 21-40 were similar at 12, 13, and 18 joules. This information supports the continued use of up to 40 fibrillation trials in canine cardiac defibrillation. However, at 7 joules defibrillation attempts 21-40 were more successful than defibrillation attempts 1-5, and 1-20. With our methodology, these data are consistent with the hypothesis that low energy shocks create a "sensitizing" effect on cardiac tissue, allowing more successful defibrillation with repeated shocks.

Animals↗

Optimizing defibrillation through improved waveforms.

Defibrillation of the heart is achieved if an electrical current depolarizes the majority of the unsynchronized fibrillating myocardial cells. The applied current or the corresponding voltage described as a function of time is called the waveform. In pacing, to stimulate myocardial cells close to the electrode, a relatively low voltage is needed for a relatively brief duration. However, in defibrillation, approximately a 100-fold higher voltage is needed and achieved by the use of capacitors. The exponential voltage decay of a capacitor during its discharge determines the basic waveform for defibrillation. In an attempt to lower the energy needed for defibrillation, the steepness of the decay (different capacitances), the duration (fixed duration waveforms) or tilt (fixed tilt waveforms), or the initial polarity can be changed. Additionally, the polarity of the electrodes can be reversed during the discharge of the capacitor once (biphasic waveform) or twice (triphasic waveform). If two capacitors and defibrillation pathways are available, bidirectional defibrillation pulses can be delivered sequentially. In humans, the original standard waveform used with endocardial leads was a single monophasic pulse delivered by a 125-microF capacitor using the endocardial right ventricular electrode as cathode. It is now known that a reversal of the initial polarity and a reversal of polarity during capacitor discharge may significantly lower the energy needed for defibrillation, thereby preventing formerly frequent failures of defibrillation with endocardial lead systems. The use of sequential pulses showed no or only slight reductions of energy requirements and was abandoned due to the additional electrode needed. The use of a smaller capacitance (60-90 microF reduced maximum energy output but generally did not reduce energy requirements for defibrillation. However, with more efficient electrodes, smaller capacitances that will help to reduce the size of the defibrillator might be used. Thus, today defibrillation is optimized with respect to energy, capacitor size, and ease of implantation if an approximately 90-microF capacitor is used to deliver a biphasic pulse via a bipolar lead system using the right ventricular electrode as anode.

Animals↗

Progressive depolarization: a unified hypothesis for defibrillation and fibrillation induction by shocks.

Experimental studies of defibrillation have burgeoned since the introduction of the upper limit of vulnerability (ULV) hypothesis for defibrillation. Much of this progress is due to the valuable work carried out in pursuit of this hypothesis. The ULV hypothesis presented a unified electrophysiologic scheme for linking the processes of defibrillation and shock-induced fibrillation. In addition to its scientific ramifications, this work also raised the possibility of simpler and safer means for clinical defibrillation threshold testing. Recent results from an optical mapping study of defibrillation suggest, however, that the experimental data supporting the ULV hypothesis could instead be interpreted in a manner consistent with traditional views of defibrillation such as the critical mass hypothesis. This review will describe the evidence calling for such a reinterpretation. In one regard the ULV hypothesis superseded the critical mass hypothesis by linking the defibrillation and shock-induced fibrillation processes. Therefore, this review also will discuss the rationale for developing a new defibrillation hypothesis. This new hypothesis, progressive depolarization, uses traditional defibrillation concepts to cover the same ground as the ULV hypothesis in mechanistically unifying defibrillation and shock-induced fibrillation. It does so in a manner consistent with experimental data supporting the ULV hypothesis but which also takes advantage of what has been learned from optical studies of defibrillation. This review will briefly describe how this new hypothesis relates to other contemporary viewpoints and related experimental results.

Animals↗

Transthoracic defibrillation of swine with monophasic and biphasic waveforms.

BACKGROUND: Biphasic waveforms have had a favorable impact on internal defibrillation but have seen minimal use in transthoracic defibrillation systems. The purpose of this study was to compare monophasic and biphasic waveforms for transthoracic defibrillation in swine. METHODS AND RESULTS: Three interrelated studies were performed in 19 swine to establish the relative transthoracic defibrillation efficacy of biphasic shock waveforms. In study 1, we measured voltage (V50) and energy (E50) strength-duration curves for monophasic and biphasic truncated exponential waveforms. We then independently examined the effects of phase duration and tilt on biphasic waveform defibrillation with a total waveform duration from study 1 that provided the minimum V50 (study 2) and the minimum E50 (study 3). At each pulse duration tested in study 1, biphasic waveforms defibrillated with significantly less voltage and energy than monophasic waveforms. At a duration of 12 ms, there was a voltage minimum for biphasic waveform defibrillation. At this duration, V50 was 1378 +/- 505 V for the biphasic waveform compared with 2185 +/- 361 V for the monophasic waveform, P = .01. For both monophasic and biphasic waveforms, E50 increased with pulse duration. With a total pulse duration of 12 ms, E50 was 169 +/- 101 J for the biphasic waveform compared with 414 +/- 114 J for the monophasic waveform, P = .003. In study 2, optimization of phase duration and total tilt reduced the defibrillation requirements of the 12-ms "minimum voltage" biphasic waveform to 1284 +/- 187 V and 129 +/- 36 J. In study 3, the 8-ms "minimum energy" biphasic waveform had an E50 of 115 +/- 35 J that was 11% less than the 12-ms biphasic waveform, P = .11; however, voltage requirements of 1476 +/- 239 V were 15% higher, P = .005. CONCLUSIONS: This study demonstrates the superiority of truncated biphasic waveforms over truncated monophasic waveforms for transthoracic defibrillation of swine. Biphasic waveforms should prove as advantageous at reducing voltage and energy requirements for transthoracic defibrillation as they have for internal defibrillation.

Animals↗

Multicenter comparison of truncated biphasic shocks and standard damped sine wave monophasic shocks for transthoracic ventricular defibrillation. Transthoracic Investigators.

BACKGROUND: The most important factor for improving out-of-hospital ventricular fibrillation survival rates is early defibrillation. This can be achieved if small, lightweight, inexpensive automatic external defibrillators are widely disseminated. Because automatic external defibrillator size and cost are directly affected by defibrillation waveform shape and because of the favorable experience with truncated biphasic waveforms in implantable cardioverter-defibrillators, we compared the efficacy of a truncated biphasic waveform with that of a standard damped sine monophasic waveform for transthoracic defibrillation. METHODS AND RESULTS: The principal goal of this multicenter, prospective, randomized, blinded study was to compare the first-shock transthoracic defibrillation efficacy of a 130-J truncated biphasic waveform with that of a standard 200-J monophasic damped sine wave pulse using anterior thoracic pads in the course of implantable cardioverter-defibrillator testing. Pad-pad ECGs were also examined after transthoracic defibrillation. After the elimination of data for 24 patients who did not meet all protocol criteria, the results from 294 patients were analyzed. The 130-J truncated biphasic pulse and the 200-J damped sine wave monophasic pulse resulted in first-shock efficacy rates of 86% and 86%, respectively (P = .97). ST-segment levels measured 10 seconds after the shock in 151 patients in sinus rhythm were -0.26 +/- 1.58 and -1.86 +/- 1.93 mm for the 130- and 200-J shocks, respectively (P < .0001). CONCLUSIONS: We found that 130-J biphasic truncated transthoracic shocks defibrillate as well as the 200-J monophasic damped sine wave shocks that are traditionally used in standard transthoracic defibrillators and result in fewer ECG abnormalities after the shock.

Adolescent↗

Strength-duration relationship for human transvenous defibrillation.

BACKGROUND: One of the basic characteristics of electrical defibrillation is the strength-duration relationship, or the effect of pulse width on defibrillation efficacy. This relationship is important for understanding the mechanism of defibrillation and for the design of optimal waveforms. However, a detailed evaluation of the strength-duration relationship for human transvenous defibrillation has not been performed previously. METHODS AND RESULTS: This was a prospective study of 29 patients undergoing initial defibrillator implantation with a uniform dual coil, transvenous lead. In each patient defibrillation thresholds were measured for either short (2, 3, 4, 6 ms) or long (6, 12, 18 ms) pulse durations, with the order of testing randomized. The shock waveform was a truncated monophasic pulse from a capacitor of 150 microF. The leading edge voltage at defibrillation threshold was 566+/-100 V for 2-ms pulses. Voltages declined exponentially with increasing pulse width reaching an asymptote by 6 ms (451+/-68 V, P<.05). Defibrillation threshold voltage was insensitive to longer pulse widths. Stored energy at defibrillation threshold showed a similar relationship with pulse width. In contrast, mean current decreased monotonically over the full range of pulse durations evaluated, and there was no evidence of a rheobase. CONCLUSIONS: The shape of the strength-duration curve and the lack of rheobase current indicate a fundamental difference between cardiac stimulation and defibrillation. The relationship between pulse duration and defibrillation threshold voltage or stored energy is well modeled by a parallel capacitor resistor circuit with a time constant of 5.3 ms.

Aged↗

Current and energy in external cardiac defibrillation.

External (Transthoracic) defibrillation is achieved by passing a large uniaxial current through the chest for a brief period of time. This current is determined by 1) the applied voltage and 2) the transthoracic impedance (TTI). In modern defibrillators the source of voltage is universally from a charged capacitor, the discharge waveform being modified in some cases by the inclusion of an inductor in the discharge circuit (Lown & Edmark waveforms, fig. 1), in others by direct discharge of a capacitor, such discharge being electrically truncated after a given period of time (Truncated Exponential, fig. 1). Although it is current that is responsible for successful defibrillation, defibrillator output is most commonly measured in units of energy (Joules) which is easily calculated knowing the voltage to which the defibrillation capacitor has been charged. Recent measurements of TTI show wide variations from 28 to 150 ohms3. Attempts at defibrillation (assuming the same energy setting) will thus result in a wide range of delivered currents. It is known that high defibrillation currents produce myocardial damage, conversely, currents which are too low will fail to achieve defibrillation. There is increasing evidence to suggest that defibrillators employing truncated exponential (trapezoidal) waveforms may be ineffective in subjects having high TTI. Additionally, there remains a need for a "smart" defibrillator which can calculate pre-discharge TTI and automatically adjust delivered current such that it is neither too low nor too high for the patient undergoing defibrillation.

Electric Countershock↗

[Electrical defibrillation and cardioversion].

Defibrillation and cardioversion are techniques in which a short electric impulse is administered to the heart in order to restore its normal rhythm. During cardioversion electric impulse is synchronized to the QRS on electrocardiogram. During defibrillation electric current passes through the heart in any phase of electric heart cycle. This mode of treatment is rather new - Lown et al. started to use it in a clinical practice in 1962. During defibrillation or cardioversion electric current goes from negative to positive electrode of defibrillator and passes the heart on its way. This induces transmembrane potential in myocardium cells and results in synchronic depolarization of all myocardium. The pathophysiology of defibrillation is explained by critical mass hypothesis as well as the upper limit of vulnerability hypothesis. The success of defibrillation depends on many factors, such as the location and size of electrodes, the type of defibrillator, the morphology of electric impulse, transthoracic impedance, the type and duration of arrhythmia. This procedure can be performed only on unconscious patient. The possible complications of the procedure can be disturbances in heart rhythm and conduction, the changes in arterial blood pressure, the damage to the myocardium, embolia, pulmonary edema and others. This article describes the mechanism of action of defibrillation and cardioversion, indications for this procedure, the technique and methods of defibrillation and cardioversion, the factors, responsible for the efficacy of the procedure and possible complications of defibrillation.

Defibrillators↗

[Atrial defibrillator].

Atrial fibrillation (AF) is a frequent and costly health care problem representing the most common arrhythmia resulting in hospital admission. Total mortality and cardiovascular mortality are significantly increased in patients with AF compared to controls. In addition to symptoms of palpitations patients with AF have an increased risk of stroke and may also develop decreased exercise tolerance and left ventricular dysfunction. All of these problems may be reversed with restoration and maintenance of sinus rhythm. External electrical cardioversion has been a remarkably effective and safe method for termination of this arrhythmia. Originally described by Lown et al. in 1963, it has been a well accepted mode of acute therapy. However, this technique requires general anesthesia or heavy sedation. Internal atrial defibrillation has been evaluated as an alternative approach to the external technique for over 2 decades. Recent studies have shown that low-energy internal atrial defibrillation using biphasic shocks is an effective and safe means in restoring sinus rhythm in patients with AF and should be considered especially in patients in whom external cardioversion attempts have failed. IMPLANTABLE ATRIAL DEFIBRILLATOR: Recently, a stand alone IAD, the Metrix System (model 3000 and 3020), has entered clinical investigation. Atrial defibrillation is accomplished by a shock delivered between electrodes in the right atrium and the coronary sinus. The right atrium lead has an active fixation in the right atrium. The coronary sinus lead has a natural spiral configuration for retention in the coronary sinus, and can be straightened with a stylet. Both leads are 7 French in diameter and the defibrillation coils are each 6 cm in length. The electrodes may be placed using separate leads, or very soon by using a single bipolar lead. A separate bipolar right ventricular lead is used for R wave synchronization and post shock pacing. The Metrix defibrillator can be used to induce AF by using R wave synchronous shocks and can store intracardiac electrograms (EGMs) for up to 2 minutes from the most recent 6 AF episodes. The device can be programmed into one of the following operating modes: fully automatic, patient activated, monitor mode, bradycardia pacing only, and off. As AF is not life-threatening, in the automatic mode the device is only intermittently active in detecting and treating AF, and this "sleep wake-up" cycle interval is programmable. The device employs extensive processing both for detection and R wave synchronization. In April 1996, the phase I Metrix multicenter clinical trial was started. As of May 1997, a total of 51 Metrix systems had been implanted as part of the phase I multicenter clinical trial. Preliminary data suggest that both defibrillation thresholds and electrograms are stable over time (implant to 3 months). Detection accuracy has been excellent (100% specificity, 92.3% sensitivity) and there have been no errors of R wave selection for synchronization. No proarrhythmias have resulted from over 3700 shocks delivered. The device is effective in electrically converting 96% of the spontaneous episodes of AF. In 27% of episodes several shocks were required because of early recurrence of AF. In 5 patients, the atrial defibrillator was removed: 2 infections, 1 cardiac tamponade, 1 permanent loss of telemetry, 1 patient required His-Bundle ablation because of frequent episodes of drug refractory AF with rapid ventricular response. Initial clinical experience under controlled conditions with the Metrix system suggests that the implantable atrial defibrillator may offer a therapeutic alternative for a subgroup of patients with drug refractory, symptomatic, long lasting, and infrequent episodes of AF. Further efforts must be undertaken to reduce the patient discomfort associated with internal atrial defibrillation in an attempt to make this new therapy acceptable to a larger patient population with AF. (ABSTRACT TRUNCATED)

Atrial Fibrillation↗

[New aspects of electric defibrillation].

Early defibrillation is the standard of care for patients with ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). Technical developments aim at further miniaturization and simplification of defibrillators as well as adaptation of energy requirements to the patient's needs. Implantable Cardioverter-Defibrillators (ICD) and automated external defibrillators (AED) are based upon the same technology. Both devices analyze the ECG signal internally, followed by a "shock" or "no shock" decision. Use of automated devices is the prerequisite for defibrillation by non-physicians. Chest impedance measurements and use of alternative shock waveforms, such as biphasic, aim at adaptation of energy or current to the patient's individual needs and avoid application of unnecessarily high amounts of energy to the myocardium. Calculation of median frequency is a non-invasive method for analyzing the heart's metabolic and electrical state. It helps to determine the optimal moment for defibrillation during cardiopulmonary resuscitation (CPR). Developments concerning the structure of in-hospital emergency systems or pre-hospital emergency medical services (EMS) aim at further reductions in time from collapse of a patient until first defibrillation. Such developments include early defibrillation programs for emergency medical technicians (EMT), nurses, and fire or police department first responders as well as wide distribution of easy-to-operate defibrillators in public areas, as discussed during the American Heart Association's Public Access Defibrillation conferences. All programs of that kind have to be organized and supervised by a physician who is responsible for training and supervision of the personnel involved.

Arrhythmias, Cardiac↗

The atrial defibrillator: a stand-alone device or part of a combined dual-chamber system?

Atrial fibrillation (AF) is an extremely common arrhythmia seen in clinical practice. Because of the limited efficacy of traditional therapeutic strategies to restore and maintain normal sinus rhythm, several nonpharmacologic options have evolved. The promising results achieved with internal atrial defibrillation have facilitated the development of an implantable atrial defibrilator. Preliminary results obtained from an initial study on a small number of highly selected patients with refractory AF suggest that atrial defibrillation can be performed effectively and safely with adequate patient tolerance by using a stand-alone device. The extension of this therapy will depend on the results of well-designed prospective studies comparing this new therapeutic option with traditional methods. Several acute studies have shown that internal conversion of AF is feasible at low energies with current endocardial transvenous lead configurations primarily designed for ventricular defibrillation, but long-term efficacy has, to date, only been demonstrated with atrial implantable defibrillator lead systems. As AF is a frequent arrhythmia in implantable cardioverter defibrillator (ICD) recipients, it would seem desirable to incorporate the capability for atrial defibrillation into an ICD. Clinical studies have shown that an atrial defibrillator, as part of a combined dual-chamber ICD system, may not require a potentially complicated switching network for establishing different electrode configurations for atrial and ventricular tachyarrhythmia. The efficacy in atrial cardioversion of such a combined, less complex device seems to be as high as reported for a pure atrial defibrillator, but generally at somewhat higher energy requirements. The results of further investigations will show whether a dual-chamber cardioverter defibrillator would be of clinical relevance in patients with ventricular and supraventricular tachyarrhythmia.

Atrial Fibrillation↗

Unique interaction between an atrial single-chamber pacemaker and a ventricular defibrillator.

A well described interaction between an antibradycardia pacemaker and a ventricular defibrillator is sensing of pacemaker stimuli by the ventricular defibrillator. This report describes an interaction between an atrial demand pacemaker and a ventricular defibrillator that resulted in ventricular asystole and polymorphic ventricular tachycardia. In this case, the ventricular defibrillator sensed atrial pacing stimuli when complete atrioventricular block with a slow ventricular escape rate developed. Defibrillator-based ventricular demand pacing was inhibited, resulting in prolonged periods of ventricular asystole, polymorphic ventricular tachycardia, and multiple defibrillator shocks. Ventricular defibrillator sensing of atrial pacemaker stimuli in the setting of complete atrioventricular block and ventricular asystole cannot be simulated during defibrillator implantation when atrioventricular conduction is intact. Therefore, a pacemaker programmed to atrial demand pacing in a patient with a ventricular defibrillator can result in inappropriate inhibition of ventricular pacing in the setting of complete heart block. Furthermore, this interaction can be avoided with a dual-chamber pacing ventricular defibrillator.

Aged↗

Quality of life and psychological impact of implantable cardioverter defibrillators: focus on randomized controlled trial data.

The defibrillator has been shown to reduce mortality in a number of patient groups with cardiac disease. Given the number of individuals with defibrillators it is important to understand the influence of these devices quality of life. Advances have led to smaller devices, less-invasive implantation, and more refined arrhythmia management. The potential impact of the defibrillator on quality of life continues to evolve with these advances. This review discusses the impact of the defibrillator on psychological well-being and quality of life, particularly the results of recent large randomized trials. Observational studies evaluating the relationship between defibrillator implantation and quality of life have not shown consistent results, but recent data from randomized trials provide important insights. Among patients who have survived life-threatening arrhythmias the defibrillator is associated with similar or perhaps superior quality of life versus antiarrhythmic drug therapy. However, patients who experience shocks have poorer quality of life versus those who do not. The reduction in quality of life with multiple shocks is of similar magnitude to serious side effects from antiarrhythmic drugs. While patients with defibrillators are at risk for poor quality of life. The advantages and disadvantages of defibrillator therapy versus amiodarone or usual medical care should be discussed with patients in whom a defibrillator is recommended. Those undergoing defibrillator implantation should be advised that adverse events and/or multiple shocks occur in a minority of patients, but may lead to reduced quality of life and it is vital that support resources be made available for these individuals.

Anti-Arrhythmia Agents↗