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PubMed1996

The implantable cardioverter defibrillator: modern implantation techniques and their impact on outcomes.

The implantable cardioverter defibrillator has revolutionized the management of lethal ventricular arrhythmias in susceptible patients. In its second decade of existence, the implantable cardioverter defibrillator has undergone significant technologic enhancements which have resulted in ease of implantation, lower mortality rates, and shorter hospital stays. The newer pectoral size devices have been successfully implanted in a variety of patients, using models from several device manufacturers. Improvements in lead technology have paralleled those of the device itself. These include the unique concept of "unipolar" defibrillation as well as the trend toward dual chamber lead systems. Results of these newer technologies are favorable: comparably low defibrillation thresholds have been reported with the newer lead configurations, with lower operative mortality. However, morbidity attached to earlier lead systems remains as high as 16%. It is anticipated that the results will further improve as shorter transvenous leads and better connector material become routinely available. Finally, the clinical outcomes in the early postoperative phase indicate fewer proarrhythmic effects leading to shorter hospital stays in patient equipped with the latest types of pectoral implants. Continued progress at the level of the patient-device interface is expected to result in every better patient acceptance and proliferation of implantable cardioverter defibrillator therapy.

Arrhythmias, Cardiac↗
PubMed1995

[Automatic implantable defibrillator and antiarrhythmic surgery in ischemic cardiopathies. Apropos of 53 cases].

The automatic implantable defibrillator (AID) and antiarrhythmic surgery are the two therapeutic options after failure of catheter ablation and/or antiarrhythmic therapy for sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) in patients with coronary artery disease. The authors undertook retrospective study of the characteristics of two groups of patients treated between November 31st 1987 et December 31st 1993 either by AID (28 men and 4 women with an average age of: 56.1 +/- 11.2 years) or by surgery (19 men and 2 women with an average age of: 60.6 +/- 6.8 years). The "surgical" patients differed from "defibrillator" patients in the fewer number of cardiac arrests, a higher proportion of sustained monomorphic VT, better tolerated sustained monomorphic VT (rarely syncopal), fewer early post-infarction arrythmias (< or = 8 weeks), more anterior wall infarction and a higher proportion of aneuvrysms. The perioperative mortality was 6.2% in the "defibrillator" group and nil in the "surgical" group (p = NS). At 2 years, the sudden death rate in the "defibrillator" and "surgical" groups was 7.5% and 0% respectively and total cardiac mortality was 17% and 20% respectively (p = NS). The authors conclude that perioperative mortality and the sudden death rate at 2 years are relatively low in the two groups. However, the total cardiac mortality remains high, largely related to perioperative death and secondary cardiac failure. Nevertheless, compared with defibrillator patients and with identical average ejection fractions, there was no extra mortality due to cardiac failure after antiarrhythmic surgery.

Aged↗
PubMed1996

Relationship of amiodarone to postoperative complications of transthoracic implantation of automatic implantable cardioverter defibrillators.

The purpose of this study is to report the results and complications associated with transthoracic placement of an implantable defibrillator and their relationship to amiodarone, and to identify clinical predictors of complications. There were 159 men and 41 women. The mean patients age was 61 +/- 11 years, and the mean ejection fraction was 0.33 +/- 0.14. Fifty one percent of patients developed complications including death in 14 patients (7%). Variables which differed in patients who died and those that did not were age, ejection fraction and New York heart failure classifications. Postoperative mortality was unrelated to amiodarone therapy. Twenty patients (10%) developed pneumonia and 15 patients (7.5%) developed respiratory failure. Clinical variables associated with the development of respiratory failure were age, amiodarone therapy and a prior history of pulmonary disease. Patients receiving amiodarone had a higher incidence of an elevated defibrillation threshold (> or = 25 joules) as compared with those not being treated with amiodarone. Clinical factors associated with an elevated defibrillation threshold were a history of a myocardial infarction, prior bypass surgery, and amiodarone. The results of this study demonstrate that placement of an implantable defibrillator using a transthoracic approach is associated with a high incidence of complications. Amiodarone therapy is associated with an increased incidence of pneumonia, respiratory failure, and elevated defibrillation thresholds.

Adolescent↗
PubMed1997

Implantable cardioverter defibrillators: physical and psychosocial outcomes.

BACKGROUND: The long-term outcomes of living with an implantable cardioverter defibrillator are an important consideration in recovery. However, little is known about physical and psychosocial outcomes beyond 1 year after implantation. OBJECTIVE: To describe the long-term physical and psychosocial adaptation of persons who have had an implantable cardioverter defibrillator for approximately 2 years or more. METHODS: This nonexperimental cross-sectional study used telephone interviews to ascertain the responses of 80 recipients of implantable cardioverter defibrillators to physical and psychosocial questionnaires to explore the long-term outcomes of living with the devices. Subjects eligible for inclusion were selected from the files of an arrhythmia clinic. RESULTS: Hierarchical regression analysis showed that subjects who are not emotional are likely to be more physically active, especially if they are young and male, and that subjects who tend to be emotional are likely to be psychologically distressed and have poorer social and domestic adaptation. Furthermore, use of emotions was a positive predictor of psychological distress and poor social and domestic adaptation. Subjects reported the use of both emotion- and problem-focused coping. Subjects' scores on physical and psychosocial functioning were comparable to scores reported in the literature for patients who have had myocardial infarction or dysrhythmia. CONCLUSIONS: Emotional responses to distress were predictive of little physical activity and psychological distress. Furthermore, young recipients of implantable cardioverter defibrillators and men were predicted to be physically active. Persons who have had an implantable cardioverter defibrillator for approximately 2 years or more can anticipate that their physical and psychosocial functioning will be similar to that of patients who have myocardial infarction or dysrhythmia.

Adaptation, Psychological↗
PubMedDate not supplied

Drug and defibrillator interactions.

We reviewed the interactions of drugs and defibrillators, with emphasis on implantable cardioverter defibrillators. Articles were identified by searching MEDLINE from 1966 to the present; additional sources were identified from reference lists in these articles. Drugs have the potential for both beneficial and harmful interactions with electrical therapy. Beneficial interactions include reductions in the energy required to defibrillate the heart and in the occurrence of arrhythmia resulting in decreased shock frequency, prolonged device longevity, and improved patient comfort. Potentially harmful interactions include altering the detection of ventricular tachycardia; altering the pacing threshold, resulting in interference with bradycardia or antitachycardia pacing; development of incessant ventricular tachycardia; and increasing the energy required to defibrillate the heart. As the use of implantable cardioverter defibrillators increases, pharmacists should be aware of the potential for drug-device interactions.

Animals↗
PubMed1998

[Dual-chamber implantable automatic defibrillators. Experiences apropos of 16 cases].

In view of the large number of inappropriate shocks observed in patients with implanted defibrillators, improved detection of ventricular arrhythmias has become a major objective. The addition of an atrial catheter has been proposed to improve discrimination between ventricular and non-ventricular arrhythmias. Besides this function, the additional catheter could be used for DDD pacing without risk of interaction between the pacemaker and defibrillator. The authors report their initial experience in 16 patients implanted with a DDD pacemaker. The indication was resuscitated sudden death (N = 5) or ventricular tachycardia (N = 11). The choice of a DDD defibrillator was justified by a bradycardia (N = 9), haemodynamic factors (N = 4) or supraventricular tachycardia (N = 3). The devices used were the Defender 9001 (ELA Medical SA, France, N = 3), the Ventak AV 1810 and the Ventak AV II DR 1821 (Guidant/CPI, Inc. USA, N = 11 and N = 2 respectively). There were three immediate complications. After 2 to 29 months' follow-up, 5 patients had received appropriate treatment by their devices. Five patients had inappropriate shocks : one patient received a shock triggered by electrical interference, two others had no active sensing algorithme when the shocks were delivered, and the other two had an activated algorithme with 1/1 conduction of a supraventricular arrhythmia. No recurrences were recorded after reprogramming the device. DDD or VDD pacing was permanent in 9 patients and intermittent in 3 others. Seven patients had dilated cardiomyopathy and severe cardiac failure and were clinically improved by dual chamber pacing. In many patients, candidates for a defibrillator, this new generation of devices has improved specificity of arrhythmia detection and cardiac pacing without risk of interaction. The authors propose a classification of the indications for a DDD defibrillator.

Algorithms↗
PubMed1995

Emergency intracardiac defibrillation for refractory ventricular fibrillation.

Hemodynamically unstable ventricular arrhythmias induced during electrophysiologic testing almost always respond to prompt application of direct current transthoracic shocks. In rare cases, however, ventricular fibrillation may be refractory to conventional treatment. Recently, a technique of intracardiac defibrillation has been successfully used to resuscitate patients with ventricular fibrillation refractory to transthoracic defibrillation. We describe two patients with a history of myocardial infarction and left ventricular dysfunction who were admitted with symptomatic episodes of ventricular tachycardia. Both had inducible sustained monomorphic ventricular tachycardia. During a repeat electrophysiologic study in Patient No. 1 on procainamide and at the initial study in Patient No. 2, right ventricular burst pacing to terminate ventricular tachycardia resulted in ventricular fibrillation refractory to resuscitation efforts, including transthoracic defibrillation with 360 J. Emergency intracardiac defibrillation with 200 and 360 J, respectively, successfully converted both patients to sinus rhythm. Both patients were subsequently discharged from the hospital on amiodarone. These cases illustrate the life-saving capabilities of intracardiac defibrillation.

Aged↗
PubMed1975

Genesis of arrhythmias and mechanism of electrical defibrillation of the heart.

Atrial arrhythmias were induced in experiments on dogs by electrical stimulation or by local application of aconitine and methacholine to the atrium. The action of the defibrillator discharge on these arrhythmias was studied. The defibrillator discharge abolished the arrhythmias maintained by the circus movement of the excitation wave over the atria but did not abolish sinus tachycardia or ectopic aconitine tachysystoles. The threshold of the defibrillating effect depends on the existence of micro-or macro-reentries. Thmechanism of defibrillation consists of excitation of the atrial myocardium with a consequent decrease in the pathway for the circulation of excitation to below the critical size for maintaining the circus movement of the excitation wave. The axtion of the defibrillator does not inihibit the automatism of the nomotopic and heterotopic cardiac pacemakers.

Aconitum↗
PubMed1995

Sotalol facilitates spontaneous ventricular defibrillation by enhancing intercellular coupling. An entirely new mechanism for its antiarrhythmic action.

We have previously shown that sotalol, a class III antiarrhythmic agent, helps spontaneous ventricular defibrillation in various mammalian species. Since we hypothesized that self ventricular defibrillation depends on a high degree of intercellular synchronization, and since the major electrophysiological action of sotalol causing prolongation of action potential duration (APD), cannot fully explain its defibrillating property, we carried out a series of studies to examine the effect of sotalol on intercellular myocardial coupling. Guinea pig right ventricular muscle preparations were superfused in a tissue bath and the spread of intracellularly injected fluorescent dye (Lucifer yellow CH) to the neighboring cells was studied under various conditions. When either the Ca2+ concentration of Tyrode's solution was elevated to 6 mM or the solution was made hypoxic by not bubbling O2 (n = 3 each), no spread of the injected dye was observed. The addition of 1 microM sotalol to the high Ca2+ solution or 0.5 microM to the hypoxic superfusate (n = 3 each) caused a wide spreading of the dye, thus strongly suggesting a marked improvement in the intercellular coupling. These results show an entirely new property of sotalol, i.e., enhancement of cellular synchronization, which may better explain its ability to cause spontaneous ventricular defibrillation than its class III action. Our previous demonstration of successful spontaneous ventricular defibrillation by several other agents that are known to enhance intercellular coupling but have contrasting actions on APD further substantiates our hypothesis.

Animals↗
PubMed2004

[Transthoracic defibrillation. Physiologic and pathophysiologic principles and their role in the outcome of resuscitation].

As one major link in the chain of survival, early transthoracic (external) cardiac defibrillation is aimed at the termination of ventricular flutter and ventricular fibrillation. Most important to the success of defibrillation is the passage of a defined amount of current through a critical mass of heart muscle. Different transthoracic resistances reduce the effective density of the current within the heart. As for other therapeutic intervention procedures, recommendations for the optimal strength of current to be applied to the fibrillating heart need to be evaluated and defined for therapeutical defibrillation too. Unnecessarily high current density causes damage to the heart and should be prevented. By using biphasic waveforms in contrast to monophasic impulses, the amount of current can be reduced but the same or even higher efficacy is attained. Therefore possible myocardial damage might be clearly reduced. Even with individually altered thoracic impedance effective conversion of cardiac rhythm can be achieved by device-controlled compensation and biphasic waveforms. According to their different mechanisms or origin (electrically induced or spontaneously caused by organic heart disease) the probability of successful conversion of the cardiac rhythm by one single electrical impulse varies. The optimum point in time for defibrillation during resuscitation needs to be redefined. In order to improve comparability, further studies should use standardized definitions for successful defibrillation relating to the resulting cardiac rhythm.

Cardiopulmonary Resuscitation↗
PubMed2006

[Public access defibrillation. Limited use by trained first responders and laymen].

As ventricular fibrillation is the most frequent initial heart rhythm causing out-of-hospital sudden cardiac arrest, defibrillation is of essential significance. Automated external defibrillators (AEDs) have been available for some years and as a result defibrillation can be carried out by individuals other than physicians and healthcare providers such as trained first responders and untrained lay rescuers. This so-called public access defibrillation nourished hope of progress in the treatment of sudden cardiac arrest. However, several limitations exist, such as low frequency of sudden cardiac arrest in public, rare use of publicly placed AEDs, low cost effectiveness, legal requirements and insufficient public willingness to help. Due to these restrictions of public access defibrillation other measures are more promising than the attempt at general distribution of AEDs. These measures are primary or secondary prophylaxis of sudden cardiac arrest, general knowledge of adequate activation of emergency medical services, implementation of first responder teams equipped with AEDs and particularly a better education in and application of the well-established principles of cardiopulmonary resuscitation.

Cost-Benefit Analysis↗
PubMed1978

Effect of pentobarbital anesthesia on ventricular defibrillation threshold in dogs.

The effect of pentobarbital anesthesia upon the minimal voltage and current required for electrical ventricular defibrillation (the defibrillation threshold) was investigated in dogs. Threshold current, energy, and charge in five dogs averaged 2 per cent, 13 per cent, and 6 per cent less under surgical levels of pentobarbital anesthesia than thresholds in the same animals in the awake, unanesthetized state. In dogs given sufficient pentobarbital to produce apnea and supported by mechanical ventilation, threshold current, energy, and charged averaged 3 per cent, 17 percent, and 2 per cent less than comparable awake values. These differences were far from statistically significant. In a second study, five dogs were kept for 8 to 10 hours at a surgical level of anesthesia with pentobarbital sodium. Defibrillation threshold current, determined at hourly intervals, did not drift outside +/-10 per cent limits. Arterial blood gas measurements revealed a stable, compensated metabolic acidosis in all animals (pH 7.36 +/- 0.06, pCO2 33 +/- 4 mm. Hg, pO2 71 +/- 9 mm. Hg). These data support the validity of defibrillation studies using animals anesthetized with pentobarbital and indicate the stability of the defibrillation threshold under controlled experimental conditions.

Anesthesia↗
PubMed1980

Therapeutic indices for transchest defibrillator shocks: effective, damaging, and lethal electrical doses.

Although prospective studies of defibrillator shock overdose cannot be performed in man, the therapeutic indices of various defibrillating current waveforms can be measured in animals. We determined the ratios TD50/ED50 and LD50/ED50 (where TD50 = median "toxic" or damage-inducing dose, ED50 = median effective or defibrillating dose, and LD50 = median lethal dose) as measures of the therapeutic index for damped sine wave defibrillator shocks in dogs. Death of an animal and/or any degree of cardiac damage found by gross or microscopic examination were defined as harmful effects of shock, analogous to drug toxicity. In terms of peak current, the ED50, TD50, and LD50 were 1.1, 5.8, and 24 amperes/kg.; the therapeutic indices were TD50/ED50 = 5 for morphologic damage and LD50/ED50 = 22 for death. In terms of delivered energy the ED50, TD50, and LD50 were 1.5, 30, and 470 joules/kg.; the therapeutic indices were TD50/ED50 = 20 for damage and LD50/ED50 = 320 for death. These data indicate a reasonable margin of safety for damped sine wave defibrillator shocks in dogs, and are consistent with reported incidences of suspected shock-induced damage in humans.

Animals↗
PubMed1986

Defibrillation with the sequential pulse technique: reproducibility with repeated shocks.

The development of the automatic implantable defibrillator has created the need to assess the effects of interventions on defibrillation success. However, first it is important to determine the spontaneous variability of defibrillation threshold (DFT) over time. We repeatedly determined DFT over a maximum of 2-1/2 hours in open-chested, halothane-anesthetized pigs. Ten seconds after induction of fibrillation, defibrillation was attempted by passing a sequential pulse shock through an indwelling catheter and patch electrodes. Ninety-seven fibrillation episodes (FEs) were induced in eight pigs, with a maximum of 30 shocks in an animal. DFT remained stable and fitted a flat least-squares regression equation (y = 6.35 + 0.0055x, where x is the ventricular FE number and y is the DFT, r = 0.0115, p = NS). The mean DFT over time for the eight animals was 7.6 +/- 1.9 J (range 4.8 to 16.3 J). The inter-animal variability for DFT was 3.7 J and the mean intra-animal DFT variability over time was 3.6 +/- 2.3 J (range 0 to 6.8 J). We conclude that, using our methodology, DFT is reproducible and consistent over at least 2 hours. This model provides the basis to assess the effects of acute interventions on the ability to defibrillate.

Anesthesia, Inhalation↗
PubMed1986

Effect of quinidine and bretylium on defibrillation energy requirements.

We examined the effect of bretylium and quinidine on the energy requirements for internal defibrillation in 14 pentobarbital-anesthetized dogs. Bretylium, 6 or 10 mg/kg (n = 6), did not affect the relation between energy and the likelihood of successful defibrillation. The mean energy required to achieve 50% success (E50) or 90% success (E90) in defibrillation was not significantly altered; E50 was 5.3 +/- 1.9 J (X +/- s.d) before and 6.1 +/- 3.5 J after bretylium (n.s.), and E90 was 7.2 +/- 2.1 J before and 8.6 +/- 3.3 J after drug (n.s.). Quinidine was administered in a series of two loading and maintenance infusions to achieve mean plasma concentrations of 2.4 +/- 0.63 and 2.95 +/- 0.88 microgram/ml, respectively (n = 8). No significant effect on defibrillation energy requirement was observed; mean E50 before and after treatment was 6.3 +/- 3.3 J and 6.2 +/- 2.9 J, respectively, and mean E90 was 8.3 +/- 4.4 J and 8.3 +/- 4.1 J, respectively. Similarly, saline administration to control dogs (n = 12) resulted in no change in E50 or E90. At concentrations or doses similar to those in patients with serious arrhythmias, neither quinidine nor bretylium appears to have consistent effects on the energy requirements for internal defibrillation in our dog model.

Animals↗
PubMed1989

Superiority of biphasic shocks in the defibrillation of dogs by epicardial patches and catheter electrodes.

Currently available internal cardiac defibrillators use a uniphasic, truncated exponential waveform morphology of about 6 msec in duration at an energy level of 23 to 33 joules. To determine if improved defibrillation could be achieved with a different waveform morphology, we implanted 4.5 cm2 titanium patches to the left and right ventricle of 28 dogs. After ventricular fibrillation was induced, defibrillation was attempted using 7, 12, 13, or 17 joules. A 5 msec rectangular uniphasic waveform morphology was compared with a 10 msec rectangular biphasic waveform with the lagging 5 msec pulse of half the amplitude of the leading 5 msec. In an additional seven dogs, a transvenous bipolar catheter was placed with the distal electrode in the right ventricular apex and the proximal electrode in the superior vena cava. Biphasic and uniphasic shocks were compared at 14 joules. In the patch-patch system, the biphasic waveform was superior to the uniphasic waveform at 7 joules (67% versus 35%, p less than 0.001) and at 12 joules (93% versus 78%, p less than 0.001). No statistically significant differences were achieved at 13 joules or 17 joules. In the catheter electrode system with a delivered energy of 14 joules, the biphasic waveform was more effective than the uniphasic waveform (87% versus 27%, p less than 0.001). Manufacturers of automatic implantable defibrillators should consider this information in the design of future automatic implantable defibrillators.

Animals↗
PubMed1991

Effects of electrophysiologic testing of the automatic implantable cardioverter-defibrillator on left ventricular systolic function and diastolic filling.

We investigated the effects of electrophysiologic testing of the automatic implantable cardioverter-defibrillator (AICD) on left ventricular systolic function and diastolic filling in 12 patients. Ventricular tachycardia or ventricular fibrillation was induced by programmed electrical stimulation and alternating-current, respectively. Patients were studied before and immediately after, 10 minutes after, and 1 hour after defibrillation by the AICD using M-mode, two-dimensional, and pulsed Doppler echocardiography. Immediately after defibrillation, increases were found in the peak early filling velocity (70 +/- 10 cm/sec to 84 +/- 24 cm/sec, p less than 0.01), peak early-to-atrial filling velocity ratio (1.05 +/- 0.21 to 1.29 +/- 0.26, p less than 0.005), and maximum rate of diastolic chamber enlargement (82 +/- 26 mm/sec to 102 +/- 44 mm/sec, p less than 0.05). These changes were not evident at 10 minutes and 1 hour. Cardiac output and ejection fraction were unchanged after defibrillation. Heart rate and diastolic filling time were unchanged. We conclude that electrophysiologic testing of the AICD does not impair left ventricular function in the immediate to 1-hour period after defibrillation. Left ventricular systolic function is unchanged and diastolic filling is enhanced.

Cardiac Pacing, Artificial↗
PubMed1991

Acute effects of intravenous propafenone on the internal ventricular defibrillation threshold in the anesthetized dog.

In 10 treated and 2 control dogs, the short-term effects of intravenous propafenone (2 mg/kg/10 minutes, followed by 1 mg/min [n = 2] or 25 micrograms/kg/min [n = 8]) on the internal ventricular defibrillation energy requirements (DER) were investigated. Multiple stored energy levels were randomly tested and the percent successful defibrillation was plotted against the stored energy, and the raw data were fit by logistic regression. The energy at 50% (E50) and 80% (E80) defibrillation success increased after propafenone by a mean of 75% (8.4 +/- 2.4 to 14.7 +/- 5.9 joules, p less than or equal to 0.05) and 59% (11.1 +/- 3.5 to 17.6 +/- 6.7 joules, p less than or equal to 0.05), respectively. Plasma propafenone levels ranged from 778 to 2554 ng/ml (1495 +/- 592 ng/ml) at the beginning to 833 to 2193 ng/ml (1297 +/- 389 ng/ml) at the end of the defibrillation trials. Two dogs served as controls and received Ringer's solution instead of propafenone and showed the temporal stability of the preparation. In conclusion, intravenous propafenone increases the internal ventricular DER in this canine model. This may have important clinical implications in patients with automatic implantable cardioverter-defibrillators (AICDs) receiving concomitant antiarrhythmic drug therapy and in patients undergoing therapy with intravenous propafenone.

Animals↗