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PubMed1999

The effects of biphasic and conventional monophasic defibrillation on postresuscitation myocardial function.

OBJECTIVES: The purpose of this study was to compare the effects of biphasic defibrillation waveforms and conventional monophasic defibrillation waveforms on the success of initial defibrillation, postresuscitation myocardial function and duration of survival after prolonged ventricular fibrillation (VF). BACKGROUND: We have recently demonstrated that the severity of postresuscitation myocardial dysfunction was closely related to the magnitude of the electrical energy of the delivered defibrillation shock. In the present study, the effects of fixed 150-J low-energy biphasic waveform shocks were compared with conventional monophasic waveform shocks after prolonged VF. METHODS: Twenty anesthetized, mechanically ventilated domestic pigs were investigated. VF was induced with an AC current delivered to the right ventricular endocardium. After either 4 or 7 min of untreated ventricular fibrillation (VF), the animals were randomized for attempted defibrillation with up to three 150-J biphasic waveform shocks or conventional sequence of 200-, 300- or 360-J monophasic waveform shocks. If VF was not reversed, a 1-min interval of precordial compression preceded a second sequence of up to three shocks. The protocol was repeated until spontaneous circulation was restored or for a total of 15 min. RESULTS: Monophasic waveform defibrillation after 4 or 7 min of untreated VF resuscitated eight of 10 pigs. All 10 pigs treated with biphasic waveform defibrillation were successfully resuscitated. Transesophageal echo-Doppler, arterial pressure and heart rate measurements demonstrated significantly less impairment of cardiovascular function after biphasic defibrillation. CONCLUSIONS: Lower-energy biphasic waveform shocks were as effective as conventional higher energy monophasic waveform shocks for restoration of spontaneous circulation after 4 and 7 min of untreated VF. Significantly better postresuscitation myocardial function was observed after biphasic waveform defibrillation.

Analysis of Variance↗
PubMed2000

New concepts in atrial defibrillation.

External cardioversion of AF is an established and accepted method for termination of individual episodes of AF. Recent advances have taken place in the area of non-pharmacologic management of AF, and despite its long history and well established technique, defibrillation has not been spared from these advances. The success of low-energy internal atrial defibrillation for the termination of both chronic and acute onset atrial fibrillation has resulted in the development of implantable defibrillators that treat this arrhythmia. Many of the advances have come about as a result of the use of defibrillation in implanted devices for recurrent AF due to the substantial efforts in an attempt to make this form of restoration of sinus rhythm more efficacious and tolerable to the patient. Additionally, the use of other non-pharmacologic control of atrial fibrillation has also been recently explored, namely the use of ablation and atrial pacing. The use of these other non-pharmacologic therapies are likely to both reduce the recurrence rate, as well as enhance the efficacy of defibrillation. However, defibrillation is likely to still be needed to terminate atrial fibrillation for persistent episodes, and its combination with these other therapies is likely synergistic. Electrical therapy to restore sinus rhythm for persistent episodes of atrial fibrillation is likely to be perceived by the patient. Therefore, the concept of patient controlled therapy from implanted devices to treat atrial fibrillation has shown promising results and will likely be a requirement of such devices in the future. Major advances in defibrillation therapy for atrial fibrillation have been made and have resulted in the development of implantable atrial defibrillators. Despite these advances in defibrillation and other therapies for atrial fibrillation, it is likely that combined pharmacologic and non-pharmacologic therapies for atrial fibrillation will prevail over the individual entities themselves. Future study is needed to determine the best therapy or combination of therapies for individual patients with atrial fibrillation.

Anti-Arrhythmia Agents↗
PubMed1987

Sequential or single pulse defibrillation? Investigations towards energy reduction in experimental animals.

With introduction of the automatic implantable cardioverter-defibrillator for treatment of medically refractory ventricular arrhythmias, many investigations are focussing on possibilities of reducing the energy necessary for defibrillating the heart to obtain a more adequate size and a longer durability of the generator. Several studies favour the sequential pulse delivery, using three electrodes, either endocardial, epicardial or subcutaneous plates, to improve defibrillation performance of low energy shocks. However, the validity of this conclusion remains equivocal since two different electrode configurations were used for single and sequential defibrillation. In the present study the influence of sequential pulse delivery, pulse sequence and resultant current pathways on defibrillation energy requirements were examined in comparison with single-shocks between the same epicardial electrode configuration as well as four orthogonally positioned patches. The energy requirement for 100% efficiency could be reduced by sequential pulsing with a time interval of 1 msec thus yielding significant superiority compared to single pulse defibrillation using three electrodes. The same reliable defibrillation and reduced threshold has been obtained by using four electrodes and one single shock. The addition of a third electrode alone had no influence on the energy requirements. Therefore, we have to discuss a different electrophysiological mechanism for sequential defibrillation than for single shocks with an extended current distribution over the heart using four electrodes. Possibly the action potential of the single cell of the fibrillating heart is of interest in reflecting the efficiency of sequential pulse defibrillation. By influencing the action potential pharmacologically in some animals, the optimal time interval for double shocks could be extended up to 7 msec.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Biphasic shocks compared with monophasic damped sine wave shocks for direct ventricular defibrillation during open heart surgery.

BACKGROUND: Biphasic waveform shocks are more effective than monophasic shocks for transchest ventricular defibrillation, atrial cardioversion, and defibrillation with implantable defibrillators but have not been studied for open chest, intraoperative defibrillation. This prospective, blinded, randomized clinical study compares biphasic and monophasic shock effectiveness and establishes intraoperative energy dose-response curves. METHODS: Patients undergoing cardiothoracic surgery with bypass cardioplegia were randomly assigned to the monophasic or biphasic shock group. Ventricular fibrillation occurring after aortic clamp removal was treated with escalating energies of 2, 5, 7, 10, and 20 J until defibrillation occurred. If ventricular fibrillation persisted, a 20-J crossover shock of the other waveform was used. RESULTS: Cumulative defibrillation success at 5 J, the primary end point of the study, was higher in the biphasic group than in the monophasic group (25 of 50 vs. 9 of 41 defibrillated; P = 0.011). In addition, the biphasic group required lower threshold energy (6.8 vs. 11.0 J; P = 0.003), less cumulative energy (12.6 vs. 23.4 J; P = 0.002), and fewer shocks (2.5 vs. 3.5; P = 0.002). Crossover-shock effectiveness did not differ between groups. Dose-response curves show biphasic shocks to have higher cumulative success rates at all energies tested. CONCLUSIONS: Biphasic shocks are substantially more effective than monophasic shocks for direct defibrillation. The dose-response curve guides selection of first-shock energy for traditional step-up protocols. Starting at 5 J optimizes for lowest threshold and cumulative energy, whereas 10 or 20 J optimizes for more rapid defibrillation and fewer shocks.

Adult↗
PubMed1990

Finite element analysis of cardiac defibrillation current distributions.

We have developed a two-dimensional finite element model of the canine heart and thorax to examine different aspects of the distribution of current through cardiac tissue during defibrillation. This model allows us to compare various electrode configurations for the implantable cardioverter/defibrillator. Since we do not yet know the electrical criteria to apply for predicting defibrillation thresholds, such as the minimum current density required for defibrillation or the critical mass if indeed such quantities are applicable, we measured defibrillation energy in dogs to determine the voltages to apply to the model for calculating current distributions. By analyzing isopotential contours, current lines, power distributions, current density histograms, and cumulative current distributions, we estimated the critical fraction and threshold current density for defibrillation, compared various electrode configurations, and assessed the sensitivity of the defibrillation threshold to electrode position, patch size, and tissue conductivity. We found that blood can shunt defibrillation current away from the myocardium, particularly in configurations using a two-electrode catheter, that myocardial tissue conductivity strongly affects the current distributions, and that epicardial patch size is more important that subcutaneous patch size. Our results are consistent with successful defibrillation requiring that 80 +/- 5% of the heart must be rendered inexcitable by a current density of 35 +/- 5 mA/cm2 or greater. This two-dimensional, isotropic model has allowed us to analyze some of the determinants of defibrillation, but more detailed interpretation of experimental data may require the extension of the model to three dimensions.

Animals↗
PubMed1993

Ventricular defibrillation in canines with chronic infarction, and effects of lidocaine and procainamide.

Prior studies in dogs with normal hearts have demonstrated that lidocaine increases but procainamide does not change the energy required for successful defibrillation. Because many postinfarct patients receiving implantable cardioverter defibrillator devices require adjunctive antiarrhythmic therapy, we have studied the effects of lidocaine and procainamide on the relationship between delivered voltage and defibrillation success in mongrel dogs 21 +/- 3 days following ligation of the left anterior descending and first diagonal coronary arteries. Internal defibrillation testing using a patch-patch electrode configuration was performed before and during the administration of saline controls (n = 10), lidocaine (n = 10) and procainamide (n = 10). The mean infarct size as determined by staining with tetrazolium was 13.4% +/- 8.3% of right and left ventricles, and did not differ significantly between groups. The 50% effective defibrillation (ED50) voltage increased with infusions of saline (16% +/- 15%), lidocaine (40% +/- 22%), and procainamide (13% +/- 15%) and the ED50 energy increased 41% +/- 44%, 104% +/- 62%, and 35% +/- 36%, respectively. However, the increase in ED50 voltages and energies were significantly greater in animals receiving lidocaine compared to those receiving either saline control or procainamide (P < 0.01). There were trends toward change of hemodynamic parameters in all animals following baseline defibrillation testing; stroke volume declined 21% +/- 16%; and mean pulmonary artery and aortic pressure increased by 22% +/- 25% and 11% +/- 15%, respectively. In conclusion, unlike our previous studies in dogs with normal hearts, in this model hemodynamic deterioration occurred with repeated fibrillation and defibrillation, and defibrillation voltage requirements increased in the control series. Taking into consideration the increase in defibrillation voltage requirements over the duration of the experiments, lidocaine increases and procainamide does not change ED50; thus, their effects are similar in normal and infarcted canine hearts.

Animals↗
PubMed1993

Transesophageal defibrillation: animal studies and preliminary clinical observations.

Ventricular fibrillation (VF) that fails to respond to transthoracic defibrillation leaves the clinician with few alternatives. The purpose of this study was to develop a technique of rescue defibrillation by use of transesophageal electrodes. Fourteen anesthetized dogs (20-30 kg) were investigated in this study. Two electrodes (300 mm2) were mounted 8 cm apart on an esophageal probe and inserted approximately 40 cm from the mouth. VF was induced using AC current delivered to the myocardium. Defibrillation was then performed between the distal electrode (anode) and anterior skin patch (cathode). After 15 seconds of induced VF, transesophageal and transthoracic defibrillation thresholds (DFTs) were determined in random order. The esophageal DFT (90 +/- 15 joules) tended to be lower than the transthoracic DFT (115 +/- 35 joules), though this difference was not statistically significant. One dog could not be defibrillated by transthoracic defibrillation but responded to transesophageal defibrillation. Esophageal electrodes were also useful for arrhythmia discrimination and ventricular pacing (pacing threshold of 38 +/- 5 mA at a pulse duration of 2.5 msec). Following transesophageal DFT determination, in ten dogs (total energy of 600 +/- 150 joules), acute esophageal histopathology demonstrated mild to severe focal injury to the mucosa and/or muscular layers. However, esophagi in four chronic dogs (total energy of 470 +/- 110 joules) showed no gross evidence of mucosal damage, perforation, or stricture 4 weeks following defibrillation. Histopathology showed only focal myocyte atrophy and repair. As a last resort, transesophageal defibrillation was performed in the emergency room on four patients with out-of-hospital refractory VF who failed > 6 high energy transthoracic shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Stability of the defibrillation probability curve with the development of ventricular dysfunction in the canine rapid paced model.

Most patients with implantable defibrillators have diminished cardiac function. Progressive heart failure might impair defibrillation efficacy, leading to interpreted device failure. This study sought to determine the effect of ventricular dysfunction on defibrillation energy using a biphasic endocardial system. Eleven dogs were ventricularly paced at 225 pulses/min for 2 weeks to induce ventricular dysfunction, and five control dogs remained unpaced. Dose response defibrillation probability curves were generated for each animal at baseline, after 2 weeks (at which time the pacemakers were turned off in the paced group), and then 1 week later. The defibrillation thresholds, ED20, ED50, and ED80 (the 20%, 50%, and 80% effective defibrillation energies, respectively) were determined for each dog at each study. In the paced dogs, the mean ejection fraction fell from 55% to 25% after pacing (P < 0.0001), and rose to 46% after its discontinuation (P = 0.0002). The defibrillation threshold, ED20, ED50, and ED80 remained unchanged in both the control and paced groups for all three studies, even after adjustment for dog weight or left ventricular mass. Rapid pacing produced no change in left ventricular mass. It induced ventricular cavity dilatation and wall thinning, which had opposing effects on defibrillation energy requirements, resulting in no net change of the ED50 in heart failure. In conclusion, the defibrillation efficacy of a biphasic transvenous system is not changed by the development of heart failure using the rapid paced canine model.

Analysis of Variance↗
PubMed1991

"Heartstart Scotland"--initial experience of a national scheme for out of hospital defibrillation.

OBJECTIVE: To determine the outcome of out of hospital defibrillation in Scotland during the year after the introduction of automated external defibrillators in October 1988. DESIGN: Retrospective analysis of ambulance service reports and hospital records. SETTING: Scottish Ambulance Service and acute receiving hospitals throughout Scotland. MAIN OUTCOME MEASURES: Delay from cardiac arrest to first defibrillator shock; vital state on arrival at hospital accident and emergency department; survival to hospital discharge. RESULTS: During the study period 268 defibrillators were purchased by public subscription and 96% of the 2000 ambulance crew underwent an eight hour training programme in cardiopulmonary resuscitation and defibrillation. A total of 1111 cardiac arrests were recorded, and defibrillation was indicated and undertaken in 602 (54%) patients, mean age 63 (range 14-92) years. A spontaneous pulse was present on arrival at hospital in 180 (30%) of the defibrillated patients, and 75 (12.5%) were subsequently discharged alive. As expected, the likelihood of survival was inversely related to the delay from the onset of cardiac arrest to the time of the first shock and was greater in the case of witnessed arrest. If ventricular fibrillation occurred after the arrival of the ambulance, survival to discharge was 33%. CONCLUSIONS: An effective scheme for out of hospital defibrillation can be introduced rapidly, and with limited training implications and costs, by the use of automated external defibrillators in ambulances.

Adolescent↗
PubMed1985

Beta-adrenergic modulation of direct defibrillation energy in anesthetized dog heart.

Catecholamines facilitate ventricular defibrillation in animals. We examined the effects of beta-adrenergic stimulation and blockade on ventricular defibrillation threshold in anesthetized dogs. Calibrated shocks were delivered between epicardial and superior vena caval electrodes, and defibrillation threshold was measured before and after administration of isoproterenol and propranolol. Eight dogs (group 1) received isoproterenol before propranolol. Nine dogs (group 2) received propranolol before isoproterenol. In group 1, the minimum energy required to defibrillate before isoproterenol was 10.6 +/- 1.7 (SE) J and decreased to 5.9 +/- 1.3 with isoproterenol (P less than 0.001). In group 2, the minimum energy required to defibrillate was 8.3 +/- 2.4 J before propranolol and increased to 10.7 +/- 2.2 after propranolol (P less than 0.001). In group 1, propranolol after isoproterenol increased defibrillation threshold (P less than 0.07), whereas in group 2 isoproterenol after propranolol produced no significant change in defibrillation threshold. Thus beta-stimulation decreased defibrillation threshold significantly in the anesthetized dog heart, an effect that was blocked by propranolol. Conversely, propranolol increased defibrillation threshold, an effect that occurred despite prior beta-stimulation, probably because of the short half-life of isoproterenol.

Animals↗
PubMed2003

Cost effectiveness of defibrillation by targeted responders in public settings.

BACKGROUND: Out-of-hospital cardiac arrest is frequent and has poor outcomes. Defibrillation by trained targeted nontraditional responders improves survival versus historical controls, but it is unclear whether such defibrillation is a good value for the money. Therefore, this study estimated the incremental cost effectiveness of defibrillation by targeted nontraditional responders in public settings by using decision analysis. METHODS AND RESULTS: A Markov model evaluated the potential cost effectiveness of standard emergency medical services (EMS) versus targeted nontraditional responders. Standard EMS included first-responder defibrillation followed by advanced life support. Targeted nontraditional responders included standard EMS supplemented by defibrillation by trained lay responders. The analysis adopted a US societal perspective. Input data were derived from published or publicly available data. Future costs and effects were discounted at 3%. Monte Carlo simulation and sensitivity analyses assessed the robustness of results. Standard EMS had a median of 0.47 (interquartile range [IQR]=0.32 to 0.69) quality-adjusted life years and a median of 14 100 dollars (IQR=8600 dollars to 21 900 dollars) costs per arrest. Targeted nontraditional responders in casinos had an incremental cost of a median 56 700 dollars (IQR=44 100 dollars to 77 200 dollars) per additional quality-adjusted life year. The results were sensitive to changes in time to defibrillation, incidence of arrest, and number of devices required to implement rapid defibrillation. CONCLUSIONS: Where cardiac arrest is frequent and response time intervals are short, rapid defibrillation by targeted nontraditional responders may be a good value for the money compared with standard EMS. The incidence of arrest should be considered when choosing locations to implement public access defibrillation.

Adult↗
PubMed1979

Determinants of ventricular defibrillation in adults.

Conventional defibrillators which stored no more than 400 J and used damped sine wave pulses defibrillated 240 of 253 (95%) episodes of ventricular fibrillation (VF) in 94 prospectively assessed resuscitations in 88 adults. Shocks of 80--240 J (under 3 J/kg) delivered to the chest wall defibrillated more often than higher energy levels. Defibrillation rate did not correlate with weight. Defibrillation was determined by the diagnosis and setting in which VF occurred. Patients with acute myocardial infarction (AMI) and primary VF or with coronary disease and no AMI defibrillated more easily than patients with AMI and secondary VF or with no coronary disease. VF in a terminal patient (agonal VF) defibrillated less often than VF in other clinical situations. Age, weight, delivered energy, duration of pulse wave, and duration of VF had little, if any, influence on rate of defibrillation. These data fail to support the use of more expensive, high-output defibrillators sold by 11 or 14 American manufactures.

Adult↗
PubMed1990

Transvenous defibrillation in humans via the coronary sinus.

A consistently effective transvenous defibrillation system for use in automatic defibrillators could significantly alter the approach to patients at risk of sudden death. Transvenous defibrillation systems that use a right ventricular (RV) electrode only or an RV electrode in combination with a chest patch are relatively inefficient at applying current to the posterolateral left ventricle. An RV electrode combined with a coronary sinus (CS) electrode, however, may improve current distribution to the posterolateral left ventricle. The purpose of this investigation, therefore, was to evaluate the effectiveness and safety of a specially designed transvenous lead system with a CS electrode capable of current delivery to this relatively inaccessible region of the heart. In 20 survivors of cardiac arrest, we determined defibrillation efficacy immediately before defibrillator surgery for monophasic pulses delivered between an RV catheter electrode and a CS catheter electrode system and compared these findings with an RV catheter electrode-thoracic patch defibrillation system. Subsequently, we referenced the efficacy of both transvenous systems to an epicardial patch electrode system at the time of defibrillator implantation. The mean delivered-energy defibrillation threshold for the CS-RV electrode system was 17.5 +/- 7.9 J, which was substantially lower than the RV electrode-thoracic patch system (25.6 +/- 11.4 J, p = 0.0016 [46% more]). Defibrillation threshold voltage was 529 +/- 123 V for the CS-RV electrode system and 647 +/- 164 V (22% more) for the RV electrode-thoracic patch system (p = 0.0013).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Vessels↗
PubMed1990

Effect of duration of ventricular fibrillation on defibrillation efficacy in humans.

The currently available automatic implantable cardioverter-defibrillator has proven highly successful for termination of ventricular tachycardia and fibrillation. Newer devices, however, permit lower energy shocks to be delivered initially and longer episodes of arrhythmia to occur before shocks are delivered. These changes may result in longer durations of arrhythmia before successful termination. Little is known about the effects of the duration of ventricular fibrillation on the efficacy of defibrillating shocks. In this study, we examined the efficacy of defibrillating shocks in 22 patients undergoing automatic implantable cardioverter-defibrillator implantation or generator change. Defibrillating shocks ranging from 300 to 600 V (5.9-24.2 J) were delivered in matched pairs after 5 and 15 seconds of ventricular fibrillation. For the 300-V shocks (5.9 J), defibrillation was accomplished in 82% of patients when the shocks were given after 5 seconds of ventricular fibrillation and in only 45% of patients when the shocks were delivered after 15 seconds (p less than 0.01). At higher energies, there was no difference in the efficacy of defibrillation shocks delivered after 5 compared with 15 seconds of ventricular fibrillation. The postshock aortic, systolic, and diastolic blood pressures were significantly lower when the shocks were given after 15 seconds of ventricular fibrillation than after only 5 seconds. We conclude that the duration of ventricular fibrillation affects defibrillation efficacy especially at energies that are relatively low compared with maximal device outputs and that longer episodes of ventricular fibrillation cause more postshock hemodynamic depression. These observations have implications for defibrillation threshold testing at the time of device implantation and for the design and programming of future automatic implantable antitachycardia devices.

Adult↗
PubMed1990

Strength-duration and probability of success curves for defibrillation with biphasic waveforms.

Certain biphasic waveforms require less energy to defibrillate than do monophasic pulses of equal duration, although the mechanisms of this increased effectiveness remain unclear. This study used strength-duration and percent success curves for defibrillation with monophasic and biphasic truncated exponential waveforms to explore these mechanisms. In part 1, defibrillation thresholds were determined for both high- and low-tilt waveforms. The monophasic pulses tested ranged in duration from 1.0 to 20.0 msec, and the biphasic waveforms had first phases of either 3.5 or 7.0 msec and second phases ranging from 1.0 to 20.0 msec. In part 2, defibrillation percent success curves were constructed for 6.0 msec/6.0 msec biphasic waveforms with a constant phase-one amplitude and with phase-two amplitudes of approximately 21%, 62%, 94%, and 141% of phase one. This study shows that if the first phase of a biphasic waveform is held constant and the second phase is increased in either duration or amplitude, defibrillation efficacy first improves, then declines, and then again improves. For pulse durations of at least 14 msec, the second-phase defibrillation threshold voltage of a high-tilt biphasic waveform is higher than that of a monophasic pulse equal in duration to the biphasic second phase (p less than 0.05), indicating that the previously proposed hypothesis of stimulation by the second phase is not the sole mechanism of biphasic defibrillation. These facts indicate the importance of the degree of tilt for the defibrillation efficacy of biphasic waveforms and suggest at least two mechanisms exist for defibrillation with these waveforms, one that is more effective for smaller second phases and another that becomes more effective as the second phase is increased.

Animals↗
PubMed1992

Clinical characteristics and outcome of patients with high defibrillation thresholds. A multicenter study.

BACKGROUND: Successful defibrillation by an implantable cardioverter-defibrillator (ICD) depends on its ability to deliver shocks that exceed the defibrillation threshold. This study was designed to identify clinical characteristics that may predict the finding of an elevated defibrillation threshold and to describe the outcome of patients with high defibrillation thresholds. METHODS AND RESULTS: The records of 1,946 patients from 12 centers were screened to identify 90 patients (4.6%) with a defibrillation threshold greater than or equal to 25 J. Excluding three patients who received ICDs that delivered greater than 30 J, there were 81 men and six women with a mean age of 59.5 +/- 10.1 years, a mean left ventricular ejection fraction of 0.32 +/- 0.14, and a 76% prevalence of coronary artery disease. Sixty-one patients (70%) were receiving antiarrhythmic drugs, and 45 (52%) were receiving amiodarone. Seventy-one patients (82%) received an ICD. Death occurred in 27 patients--19 of the 71 (27%) with an ICD (eight arrhythmic), and eight of the 16 (50%) without an ICD (four arrhythmic). Actuarial survival for all patients at 5 years was 67%. Actuarial survival rates at 2 years for patients with and without an ICD were 81% and 36%, respectively (p = 0.0024). Actuarial survival at 5 years for the ICD patients was 73%; no patient without an ICD has lived longer than 32 months. Actuarial survival free of arrhythmic death in the ICD patients at 5 years was 84%. Although the only variable to predict survival was ICD implantation (p = 0.003), it is entirely possible that in this retrospective analysis, clinical selection decisions to implant or to not implant an ICD differentiated patients destined to have better or worse outcomes, respectively. CONCLUSIONS: Antiarrhythmic drug use may be causally related to the finding of an elevated defibrillation threshold. When patients with high defibrillation thresholds receive an ICD, arrhythmic death remains an important risk (42% of deaths in these patients were arrhythmia related, with 16% actuarial incidence at 5 years). Vigorous testing to optimize patch location can potentially benefit patients by enhancing the margin of safety for effective defibrillation.

Adult↗
PubMed1997

Pinacidil's Effects on Defibrillation Outcomes: Role of Increased Potassium Conductance Via the K(ATP) Channel.

BACKGROUND: It has been shown that the inhibition of potassium ion conductance decreases defibrillation threshold. We postulated that if potassium conductance is a primary mechanism affecting defibrillation threshold values, then increasing potassium ion conductance will increase defibrillation values. The primary objective of this study was to determine if the ATP-dependent potassium (K(ATP)) channel opener pinacidil would increase defibrillation threshold values. The second objective was to prove that the observed changes were due to potassium conductance by using the K(ATP) inhibitor, glyburide, to reverse the electrophysiologic actions of pinacidil. The third objective was to determine if the electrophysiology action sof pinacidil correlate with changes in defibrillation threshold value. METHODS AND RESULTS: Domestic farm swine (n = 14) were anesthetized and intubated. Subsequently, they were instrumented with monophasic action potential catheters and epicardial defibrillation patches. Defibrillation threshold values, action potential duration, effective refractory period, and ventricular fibrillation cycle length were determined at baseline and during treatment phase 1 and treatment phase 2. Pigs were randomized into 2 groups: group 1 (n = 6) received D(5)W in treatment phase one followed by D(5)W in treatment phase 2 and group 2 (n = 8) received pinacidil in treatment phase one followed by the addition of glyburide in treatment phase two. DFT(ED50) did not change at baseline, treatment phase one or treatment phase two for group 1 (10.5 +/- 2, 11.1 +/- 1.7, 10.5 +/- 1.0 J) or for group 2 (10.1 +/- 2.2, 11.4 +/- 4.2, 11.4 +/- 3.0 J). Electrophysiologic parameters )QRS, effective refractory period, action potential duration(90), and ventricular fibrillation cycle length) were not significantly changed from baseline in group 1. In contrast, effective refractory period, action potential duration(90), and ventricular fibrillation cycle length significantly decreased at all recorded sites after the administration of pinacidil in group 2 (range of 7-13%, 6-9%, and 12-17%, respectively). However, pinacidil did not change the basal level of dispersion in effective refractory period, action potential duration, and ventricular fibrillation cycle length during paced rhythm or ventricular fibrillation. Glyburide reversed pinacidil's electrophysiologic actions. CONCLUSIONS: Pinacidil does not alter defibrillation threshold, but it reduces effective refractory period, action potential duration, and ventricular fibrillation cycle length and does not increase electrical heterogeneity. Therefore, changes in potassium channel conductance as well as shortening repolarization are unlikely primary mechanisms for elevating defibrillation threshold.

Journal Article↗
PubMed1992

[Implantable defibrillators].

Automatic implantable defibrillator therapy has changed the approach to life-threatening ventricular tachycardia completely and essentially improved survival after aborted sudden cardiac death. Since the first implantation of a defibrillator in 1980, 20,000 patients have received such a device. Nonetheless, in Germany still too many patients die of sudden cardiac death because defibrillator therapy fails to be known enough and keeps not being made use of (no more than 1,000 implants to date). In this group of patients characterized by poor ventricular function, antiarrhythmic drug therapy proved to be unreliable or even dangerous in many cases, while electrophysiologically-guided surgical interventions use to be impossible. The introduction of the implantable defibrillator enabled the incidence of sudden cardiac death to be reduced to about 2% during the first year after implant, and to 5% in the third year, respectively. In most centers with more extensive experience in defibrillator implantations, operative mortality is about 2-3%. Long-term results with defibrillator patients are controlled by the course of the underlying disease, which is coronary artery disease with large scars due to infarction in some 75% of cases. In a large group of about 10,000 patients, total mortality has been calculated to be 15% after three years. Defibrillator systems of the latest generation offer multiple programmability of tachycardia identification parameters and permit differentiated modification of therapeutic intervention. Defibrillator therapy has now been improved essentially by the introduction of endocardial lead systems and, in addition, by the defibrillator being combined with an antitachycardia pacing system.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗