Direct comparison of monophasic, biphasic and sequential pulse defibrillation over a single current pathway.

BACKGROUND: Defibrillation waveform and its spatial and temporal distribution are important determinants of its efficacy. Previous comparisons of monophasic, biphasic and sequential waveforms have used one current pathway for monophasic and biphasic defibrillation and two pathways for sequential defibrillation thus confounding a direct comparison of the waveforms. DESIGN: This study compared monophasic, biphasic and sequential pulse defibrillation over a single current pathway using a nonthoracotomy and a thoracotomy lead system in a dog model. MAIN RESULTS: Eight mongrel dogs (mean weight 21.6+/-2.9 kg) first underwent nonthoracotomy defibrillation testing followed by a median sternotomy and implantation of two 13.9 cm2 epicardial patch electrodes posterior = cathode). Nonthoracotomy electrode configuration consisted of a right ventricular catheter (cathode) and a chest wall subcutaneous patch (anode). After 10 s of alternating current induced ventricular fibrillation, defibrillation was attempted with a test shock. Monophasic, biphasic and sequential shocks of 10 ms total duration were compared. Biphasic and sequential shocks consisted of two 5 ms components separated by 0.25 ms switch time constant. Four trials of five leading edge voltages were performed for each waveform and stepwise logistic regression analysis was used to determine 80% probability of successful defibrillation (E80). For epicardial defibrillation, E80s were monophasic 11.3+/-1.5 J; biphasic 7.9+/-1.2 J; and sequential 12.1+/-1.4 J. For nonthoracotomy defibrillation, E80s were monophasic 17.7+/-3.4 J; biphasic 13.8+/-3.3 J; and sequential 18.2+/-3.5 J. The mean E80 for biphasic pulses was significantly lower than monophasic or sequential pulses for either lead system. CONCLUSIONS: Biphasic pulses are superior to monophasic or sequential pulses delivered over a single current pathway.

A direct comparison of epicardial and nonthoracotomy defibrillation using monophasic and biphasic shocks.

Defibrillation using epicardial patches may be associated with lower energy requirements than nonthoracotomy defibrillation although a direct comparison using various waveforms has not been reported. To directly compare defibrillation efficacy using these two configurations, nine mongrel dogs (20.9 +/- 2.3 kg) first underwent nonthoracotomy defibrillation testing followed by a thoracotomy and implantation of epicardial patch electrodes and redetermination of defibrillation efficacy. Each dog served as its own control. Nonthoracotomy electrode configuration consisted of a right ventricular catheter (cathode) and a chest wall subcutaneous patch (anode). The epicardial configuration consisted of two 13.9 cm2 epicardial patches. Alternating current induced ventricular fibrillation was allowed to persist for 10 seconds, followed by either a monophasic or a single capacitor biphasic shock of 10-msec total duration. Four trials of five leading edge voltages were performed for monophasic and biphasic pulses and stepwise logistic regression analysis was used to determine 80% probability of successful defibrillation (E80). For epicardial defibrillation E80s were: monophasic 19.2 +/- 4.2 J and biphasic 12.6 +/- 4.0 J; nonthoracotomy defibrillation E80s were: monophasic 24.2 +/- 4.4 J and biphasic 17.8 +/- 4.1 J. Epicardial patch defibrillation required less energy than nonthoracotomy electrode configuration. However, using biphasic pulses nonthoracotomy defibrillation could achieve lower defibrillation energy requirements than epicardial defibrillation with monophasic pulses.

Electrode polarity is an important determinant of defibrillation efficacy using a nonthoracotomy system.

Experimental and clinical data using epicardial patch electrodes and monophasic waveform suggest that electrode polarity may be an important determinant of defibrillation efficacy. Our objective was to examine the effect of electrode polarity in an animal model using a nonthoracotomy system and monophasic and biphasic waveforms for defibrillation. We examined the effect of lead polarity in 14 pentobarbital anesthetized dogs (21.1 +/- 2.4 kg) using monophasic and biphasic shocks and a nonthoracotomy system. Monophasic and single capacitor biphasic shocks of 10-msec total duration were used. The lead system consisted of a right ventricular catheter electrode with 4-cm2 surface area and a left chest wall subcutaneous patch electrode with 13.9-cm2 surface area. Electrode polarities RV(-)-Patch(+) and RV(+)Patch(-) were tested using both monophasic and biphasic waveforms. Alternating current was used to induce ventricular fibrillation and test shocks were delivered after 10 seconds of ventricular fibrillation. Each polarity configuration for monophasic and biphasic waveforms was tested four times at five different capacitor voltage levels (200-600 V, in 100-V increments). Defibrillation efficacy curves were constructed using logistic regression analysis for each animal and energies associated with 80% probability of successful defibrillation (E80) were determined. The mean E80 +/- SD values were as follows. Monophasic waveform: RV(-)Patch(+) 23.4 +/- 7.5 J; RV(+)Patch(-) 20.9 +/- 7.9 J (P < 0.03). Biphasic waveform: RV(-)Patch(+) 15.8 +/- 6.8 J; RV(+)Patch(-) 12.5 +/- 6.0 J (P < 0.03). The mean impedance values for both waveforms using either polarity ranged from 65.4 to 67 ohms and were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Pericardial effusion increases defibrillation energy requirement.

Pericardial effusion may increase defibrillation energy requirements. We examined the effect of pericardial effusion in seven pentobarbital anesthetized dogs (25.3 +/- 3.4 kg) using monophasic and biphasic shock. A median sternotomy was performed and two 13.9 cm2 patch electrodes were sewn extrapericardially; 3 cc/kg of 0.9% NaCl was instilled through an intrapericardial catheter used to create a hemodynamically insignificant pericardial effusion. Four trials of five leading edge voltages (200-600 volts, in 100 volt increments) were performed for monophasic and biphasic shocks of 10 msec total duration and defibrillation efficacy curves were determined by logistic regression analysis. Baseline impedance was 68.1 and 66.2 Ohms for monophasic and biphasic waveforms, respectively, and decreased to 52.9 and 49.9 Ohms, respectively, with pericardial effusion (P < 0.01). Energy associated with 80% probability of successful defibrillation (E80) for monophasic shock was 16.0 joules at baseline and increased to 18.5 joules with pericardial effusion (P < 0.016). Similarly, E80 for biphasic shocks increased from 10.6 joules to 13.0 joules (P < 0.016). Removal of pericardial effusion was associated with impedance and E80 returning to baseline. In this model, pericardial effusion increased defibrillation energy requirements and may explain early postimplant defibrillator failure.

Use of intravenous esmolol to predict efficacy of oral beta-adrenergic blocker therapy in patients with neurocardiogenic syncope.

The usefulness of esmolol in predicting the efficacy of treatment with an oral beta-adrenergic blocking agent was evaluated in 27 consecutive patients with neurocardiogenic syncope. Seventeen patients had a positive head-up tilt test response at baseline and 10 patients required intravenous isoproterenol for provocation of hypotension. All patients were then given a continuous esmolol infusion (500 micrograms/kg per min loading dose for 3 min followed by 300 micrograms/kg per min maintenance dose) and rechallenged with a head-up tilt test at baseline or with isoproterenol. Of the 17 patients with a positive baseline tilt test response, 11 continued to have a positive response to esmolol challenge. Sixteen patients (including all 10 patients with a positive tilt test response with isoproterenol) exhibited a negative response to upright tilt during esmolol infusion. Irrespective of their response to esmolol infusion, all patients had a follow-up tilt test with oral metoprolol after an interval of greater than or equal to 5 half-lives of the drug. All 16 patients (100%) with a negative tilt test response during esmolol infusion had a negative tilt test response with oral metoprolol. Of the 11 patients with a positive tilt test response during esmolol infusion, 10 (90%) continued to have a positive response with oral metoprolol. It is concluded that in the electrophysiology laboratory, esmolol can accurately predict the outcome of a head-up tilt response to oral metoprolol. This information may be helpful in formulating a therapeutic strategy at the initial head-up tilt test in patients with neurocardiogenic syncope.

Role of implantable cardioverter defibrillator therapy in the management of high-risk patients.

Cardiovascular mortality from ventricular tachycardia (VT) and ventricular fibrillation (VF) continues to be a major health problem. Several therapeutic approaches are now available to treat patients with known VT/VF. Among the various therapeutic options are antiarrhythmic drugs, catheter or surgical ablation of VT focus, and implantable cardioverter defibrillator (ICD). The overall 2-year cardiovascular mortality is significantly reduced by ICD therapy. The ICD is particularly useful in patients with 1) no inducible but clinical VT/VF, 2) drug refractory VT/VF, and 3) VT/VF in association with left ventricular ejection fraction of less than or equal to 30%. Significant improvements in ICD therapy have already been made; these improvements include tiered antitachycardia therapy, antibradycardia pacing, lower defibrillation threshold, and longer life of generator. Further improvements are expected, including nonthoracotomy approach to defibrillation, pectoral implant, and dual chamber sensing. It is likely that with all of the advances in ICD therapy its acceptance as a therapeutic option will increase.

When is it safe not to replace an implantable cardioverter defibrillator generator?

In most reports on patients receiving implantable cardioverter defibrillators, shocks were received mainly during the first 2 to 3 years. Thus, the question had been raised as to the need for device replacement after 3 or 4 years if no shocks had been received. In order to answer this question, shock experience in 184 patients receiving the implantable cardioverter defibrillator was analyzed. Patients were followed for a mean of 24 +/- 18.7 months. A patient's shock was judged to be appropriate if there was electrocardiographic documentation of sustained ventricular tachyarrhythmia at the time of shock or if it was preceded by sudden onset of presyncopal or syncopal symptoms. The majority of patients had coronary artery disease. In approximately two-thirds of patients, left ventricular ejection fraction was below 40%. One hundred fourteen patients had inducible sustained monomorphic ventricular tachycardia. On follow-up, there were 29 deaths, five of which were sudden. Sixty-eight patients received an appropriate shock during follow-up (37%). Over 90% of these 68 received their first shock within the 2 years after implant. The actuarial risk of receiving an appropriate shock by the fifth year after implant was 69%. Conversely, 31% of patients who survived 5 years had not received an appropriate shock. Hazard analysis indicates that there is a high incidence of first appropriate shock during the year following implant. Subsequently, the incidence dropped to a relatively steady rate with a rise in this rate during the fifth year. This analysis suggested a bimodal distribution of appropriate shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Does reception of appropriate shocks from the implantable cardioverter defibrillator affect survival?

The implantable cardioverter defibrillator has become an important therapeutic modality for treatment of life-threatening ventricular tachyarrhythmias. Recent reports have suggested that patients who receive appropriate shocks from this device have an inordinately high overall mortality, and questioned the extent of benefit these patients derive from the implant. This report analyzed the survival among 184 patients who received the implantable cardioverter defibrillator to assess survival differences between patients who received appropriate shocks versus those who did not. At a mean follow-up of 24 +/- 18.7 months, 68 patients received an appropriate shock from their device while 116 did not receive an appropriate shock. Overall survival of the entire population was quite similar to those published by others. There was no significant difference between overall survival of patients who received an appropriate shock versus those who did not. However, there was a statistically significant difference in sudden death mortality. The group of patients that received appropriate shocks included all five sudden deaths. This observation suggested that sudden death in this population was likely due to ventricular tachyarrhythmias rather than strictly bradycardia or asystole. The "benefit" of the device to the entire population was also assessed by estimating survival after receipt of the first appropriate shock. Using this approach, an estimated 10% of patients died without receiving an appropriate shock. In other words, ultimately, 90% of patients were expected to benefit from the device. This survival curve, which initiated only after receipt of the first appropriate shock was fairly similar to those estimated from conventional methods. Therefore, survival after receipt of an appropriate shock was comparable to overall survival and there was no significant difference between survival of patients who received appropriate shocks and those who did not.

Comparison of efficacy of automatic implantable cardioverter defibrillator in patients older and younger than 65 years of age.

PURPOSE: The efficacy of the automatic implantable cardioverter defibrillator (AICD) was compared in elderly patients and younger patients with life-threatening ventricular tachyarrhythmias. Clinical characteristics, surgical complications, and long-term survival rates were compared between the two age groups. PATIENTS AND METHODS: A retrospective study was conducted of 54 elderly patients (greater than 65 years) and 79 younger patients (less than 65 years) who had had AICDs implanted for recurrent symptomatic ventricular tachycardia and/or ventricular fibrillation. RESULTS: In 85% of elderly patients and 78% of younger patients, coronary artery disease was the underlying disease (NS). The mean left ventricular ejection fraction was 31.4 +/- 14.3% in the elderly patients and 35.7 +/- 17.6% in the younger patients (NS). Concomitant myocardial revascularization was performed in 37% of elderly patients and 29% of younger patients (NS); however, only 4% of elderly patients had concomitant left ventricular resection or cryoablation, compared with 15% of younger patients (p less than 0.001). Two patients in each age group died perioperatively (4% versus 3%, NS), and no significant difference in surgical morbidity or length of hospital stay following AICD implantation was noted between the age groups. In conjunction with AICD, elderly patients more commonly received antiarrhythmic drugs, with 54% of elderly patients taking amiodarone at the time of hospital discharge compared with 29% of the younger patients (p less than 0.008). In contrast, beta-blockers were more commonly used in younger patients (16% versus 2%, p less than 0.03). At a mean follow-up of 25 months, 11 (20%) elderly patients and 16 (20%) younger patients had died. Six deaths in elderly patients and five deaths in younger patients were classified as arrhythmic deaths (NS); however, only one younger patient and three elderly patients died suddenly (NS). Calculated survival curves demonstrated similar survival rates in the two age groups with approximately 90%, 87%, and 80% of the patients alive at 1, 2, and 3 years, respectively. Theoretic survival curves calculated from appropriate AICD shocks demonstrated significantly lower survival compared with actual survival. CONCLUSION: It is concluded that AICD is a very effective treatment for life-threatening ventricular tachyarrhythmias, and this benefit applies to elderly patients as well as younger patients.

Unexplained syncope evaluated by electrophysiologic studies and head-up tilt testing.

OBJECTIVE: To determine the clinical characteristics of subgroups of patients with unexplained syncope having electrophysiologic studies and head-up tilt testing and to assess the efficacy of various therapies. DESIGN: Retrospective study. SETTING: Inpatient services of a tertiary referral center. PATIENTS: Eighty-six consecutively referred patients with unexplained syncope. MEASUREMENTS: All patients had electrophysiologic examinations. Patients with negative results subsequently had head-up tilt testing. MAIN RESULTS: Twenty-nine (34%) patients (group 1) had abnormal electrophysiologic results, with sustained monomorphic ventricular tachycardia induced in 72%. Thirty-four (40%) patients (group 2) had syncope provoked by head-up tilt testing. The cause of syncope remained unexplained in 23 (26%) patients (group 3). Structural heart disease was present in 76%, 6%, and 30% of groups 1, 2, and 3, respectively. In group 1, pharmacologic or nonpharmacologic therapy was recommended based on electrophysiologic evaluation. All group 2 patients had negative results on head-up tilt testing while receiving oral beta blockers (27 patients) or disopyramide (7 patients). Group 3 patients did not receive any specific therapy. During a median follow-up period of 18.5 months, syncope recurred in 9 (10%) patients. CONCLUSIONS: The combination of electrophysiologic evaluation and head-up tilt testing can identify the underlying cause of syncope in as many as 74% of patients presenting with unexplained syncope. Therapeutic strategies formulated according to the results of these diagnostic tests appear to prevent syncope effectively in most patients.

Coronary artery fistula formation secondary to permanent pacemaker placement.

We present the findings in two patients who apparently developed a coronary artery fistula as a complication of an endocardial pacing electrode. This complication may actually be occurring more frequently than recognized because the patient may be asymptomatic or minimally symptomatic and therefore not undergo a coronary angiogram. Awareness of this potentially serious complication is important and stresses the need for proper electrode placement without excess pressure on the tip.

Sudden cardiac death: management of high-risk patients.

Sudden cardiac death remains a leading cause of death in the United States, accounting for more than 350,000 deaths each year, and the survival rate of victims remains low. Most survivors face a significant risk for recurrence. The typical substrate is chronic--abnormal myocardium with fibrosis (often from previous myocardial infarction) and left ventricular dysfunction. Acute triggers for sudden cardiac death are primarily electrical, ischemic, metabolic, neurohormonal, and pharmacologic. In most electrocardiographically documented cases of sudden cardiac death, the trigger-substrate interaction appears to result in ventricular tachycardia and fibrillation. After initial resuscitation, survivors need a thorough cardiovascular evaluation, including definition of coronary anatomy, left ventricular function, and wall-motion abnormalities, as well as an electrophysiologic evaluation. An attempt must be made to determine what each survivor's correctable triggers are. Management should address all reversible triggers, such as acute ischemia and electrolyte abnormalities, and should include modifying or correcting the arrhythmogenic substrate. Empiric antiarrhythmic therapy offers no advantage in such modification. Pharmacologic therapy with antiarrhythmic drugs should be guided by an objective therapeutic endpoint, which is best accomplished through the use of programmed ventricular stimulation and serial electrophysiologic studies. Other therapeutic options include surgical suppression of ventricular tachycardia and implantation of a cardioverter defibrillator.

Automatic implantable cardioverter/defibrillator discharges and acute myocardial injury.

Multiple defibrillations by the automatic implantable cardioverter/defibrillator (AICD) have been reported to result in localized epicardial damage. No data exist, however, regarding whether this damage can be detected in the clinical setting or whether it interferes with the detection of true myocardial infarction. Forty-nine patients who received defibrillations by patch electrodes were studied prospectively. We attempted to document the presence of myocardial injury with the following three commonly used modalities for the detection of myocardial infarction: serial electrocardiographic changes, serial creatine phosphokinase (CPK) and CPK-MB release, and technetium 99m pyrophosphate scanning. Fifteen patients received defibrillations by AICD patches at the time of AICD generator replacement. Nine patients received defibrillations at the time of new AICD lead placement. The average total energy delivered was 85 +/- 29 J. None of these patients had detectable myocardial injury. Ten patients had defibrillations by the AICD patches at the time of bypass operation. One patient in this group developed acute myocardial infarction in the inferior wall after posterior descending coronary bypass operation, as detected by electrocardiogram, 99mTc pyrophosphate scanning, and CPK-MB analysis. Fifteen patients were evaluated for spontaneous AICD discharges. Thirteen had a maximum of five consecutive shocks, and cumulative energy delivered was not greater than 330 J. None of these patients had detectable injury. Two patients had CPK-MB release of 15.3% and 7.5%, respectively. One of these patients had a positive 99mTc pyrophosphate scan. These two patients received 12 and 17 rapid and consecutive AICD discharges, respectively, with cumulative delivered energy of 360 and 510 J, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Early development of defibrillation devices.

The recognition of ventricular fibrillation and the development of defibrillation devices are recounted, and recent advances are described. Early experiences with and studies of cardiac arrest are discussed. Transthoracic defibrillation, which was first applied successfully in 1947, is reviewed, and significant research is summarized. The development and present state of the implanted defibrillator, which was suggested in the late 1960s, are examined.

Comparison of monophasic with single and dual capacitor biphasic waveforms for nonthoracotomy canine internal defibrillation.

Monophasic and single capacitor and dual capacitor biphasic truncated exponential shocks were tested in pentobarbital-anesthetized dogs with use of a nonthoracotomy internal defibrillation pathway consisting of a right ventricular catheter electrode and a subcutaneous chest wall patch electrode. Seven dogs weighing 20.2 +/- 0.5 kg were utilized. Monophasic pulses of 10 ms duration were compared with three biphasic pulses. All biphasic waveforms had an initial positive phase (P1) followed by a terminal negative phase (P2) and the total duration of P1 plus P2 was 10 ms. The dual capacitor biphasic waveform (P1 9 ms, P2 1 ms) had equal initial voltages of P1 and P2. Two simulated single capacitor biphasic waveforms were also tested, the first designed to minimize the magnitude of P2 (P1 9 ms, P2 1 ms with initial voltage of P2 equal to 0.3 of the initial voltage of P1) and the second to maximize P2 (P1 5 ms, P2 5 ms with initial voltage of P2 = 0.5 P1). Alternating current was used to induce ventricular fibrillation and four trials of eight initial voltages from 100 to 800 V were performed for each of the four waveforms. Stepwise logistic regression was utilized to construct curves relating probability of successful defibrillation and energy. In the logistic model, the dual capacitor biphasic and single capacitor biphasic waveforms that maximized P2 were associated with significantly (p less than 0.001) lower energy requirements for defibrillation than those of the monophasic waveform. The single capacitor biphasic waveform that minimized P2 was not significantly better than the monophasic waveform.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term internal cardiac defibrillation threshold stability.

The automatic implantable cardioverter-defibrillator is tested intraoperatively with defibrillation trials to ensure effectiveness. It is unknown if the energy requirement for internal defibrillation remains stable and that once demonstrated effective, if the device will continue to be effective in terminating lethal ventricular arrhythmias. In this study, the defibrillation energy requirement was compared in 56 patients at the time of lead implantation to that obtained at the time of generator replacement. Mean time to generator replacement was 17. +/- 6.6 months. The defibrillation threshold was stable over that time (11.9 +/- 6.7 joules compared to 12.7 +/- 8.4 joules, NS). There was no relation between transmyocardial impedance and defibrillation threshold. In addition, no effect on defibrillation threshold was demonstrated by the use of various cardiac medications, concomitant surgery or the occurrence of clinical shocks during follow-up.

Complications of automatic implantable cardioverter defibrillators: radiographic, CT, and echocardiographic evaluation.

Automatic implantable cardioverter defibrillators (AICDs) were studied in three groups: (a) Serial radiographs were reviewed in 51 clinic patients. Twenty of 96 (21%) AICD patches distorted with time. (b) Thirty-six postoperative computed tomographic (CT) scans of asymptomatic patients revealed that pericardial fluid collections were frequent during the month after surgery but rare beyond that. Echocardiography was insensitive for these collections. CT also demonstrated dense fibrosis around some distorted patches, months after surgery. (c) Five other patients with pericardial infection had distorted patches, and the four studied with CT had fluid beneath their patches. (d) A case of constrictive pericarditis had distorted patches but was not diagnosed with CT. The authors conclude that distorted patches may indicate postoperative complications and that CT is the imaging modality of choice.

Comparative efficacy of monophasic and biphasic truncated exponential shocks for nonthoracotomy internal defibrillation in dogs.

Pentobarbital-anesthetized dogs were studied to determine the relative efficacy of monophasic and biphasic truncated exponential shocks employing a nonthoracotomy internal defibrillation pathway that consisted of a right ventricular catheter electrode (cathode) and a subcutaneous chest wall patch electrode (anode). In part 1 of the experiments, six dogs (19.6 +/- 1.1 kg) were utilized. Monophasic pulses of 5, 7.5, 10 and 12.5 ms duration were compared with biphasic pulses of the same total duration. The biphasic pulses had an initial positive phase (P1) followed by a terminal negative phase (P2) with the initial voltage equal for each phase. For each biphasic total pulse width, five relative P1 versus P2 durations were tested (50 and 50%, 75 and 25%, 90 and 10%, 25 and 75%, 10 and 90%). Ventricular fibrillation was induced by alternating current and pulse configurations were tested randomly to determine the minimal voltage and energy for defibrillation (threshold). Biphasic shocks with P1 longer than P2 were associated with significantly lower (p less than 0.01) energy thresholds than were monophasic shocks. Additionally, there was no significant relation between pulse width and voltage or energy thresholds. In part 2 of the experiments, six dogs (20.2 +/- 1.6 kg) were studied. Monophasic shocks were compared with biphasic shocks with P1 versus P2 durations of 75 and 25% and 90 and 10% for total pulse widths of 7.5, 10 and 12.5 ms. Threshold determinations were performed as in part 1. Subsequently, five initial voltages clustered about threshold were randomly tested four times and dose-response curves constructed for each pulse configuration with the use of stepwise logistic regression. Biphasic shocks resulted in significantly lower energy (p less than 0.0001) and voltage (p less than 0.001) requirements than did monophasic shocks.(ABSTRACT TRUNCATED AT 250 WORDS)