Defibrillation Threshold Values Research Articles

Defibrillation Threshold Testing and Long-term Follow-up in Chagas Disease.

Sudden cardiac death is the most common cause of death in chronic Chagas cardiomyopathy (CCC). Because most CCC patients who are candidates for implantable cardioverter-defibrillators (ICD) meet criteria for high defibrillation threshold values, a defibrillator threshold test (DTT) is suggested. We investigated the use of DTT in CCC patients, focusing on deaths related to ICD and arrhythmic events, as well as treatment during long-term follow-up. We retrospectively evaluated 133 CCC patients who received an ICD mainly for secondary prevention. Demographic, clinical, laboratory data, Rassi score, and DTT data were collected, with p < 0.05 considered significant. The mean patient age was 61 (SD, 13) years and 72% were men. The baseline left ventricular ejection fraction was 40 (SD, 15%) and the mean Rassi score was 10 (SD, 4). No deaths occurred during DTT and no ICD failures were documented. There was a relationship between higher baseline Rassi scores and higher DTT scores (ANOVA = 0.007). The mean time to first shock was 474 (SD, 628) days, although shock was only necessary for 28 (35%) patients with ventricular tachycardia, since most cases resolved spontaneously or through antitachycardia pacing. After a mean clinical follow-up of 1728 (SD, 1189) days, 43 deaths occurred, mainly related to progressive heart failure and sepsis. A routine DTT may not be necessary for CCC patients who receive an ICD for secondary prevention. High DTT values seem to be unusual and may be related to high Rassi scores.

Defibrillation threshold of internal cardioversion prior to ablation predicts atrial fibrillation recurrence.

BackgroundMany studies have reported the predictors of atrial fibrillation (AF) recurrence after persistent AF (peAF) ablation. However, the correlation between the atrial defibrillation threshold (DFT) for internal cardioversion (IC) and AF recurrence rate is unknown. Here we investigated the relationship between the DFT prior to catheter ablation for peAF and AF recurrence.HypothesisDFT prior to ablation was the predictive factor for AF recurrence after peAF ablation.MethodsFrom June 2016 to May 2019, we enrolled 82 consecutive patients (mean age, 65.0 ± 12.4 years), including 45 with peAF and 37 with long‐standing peAF, at Hamamatsu Medical Center. To assess the DFT, we performed IC with gradually increasing energy prior to radiofrequency application.ResultsForty‐nine and 33 patients showed DFT values less than or equal to 10 J (group A) and greater than 10 J or unsuccessful defibrillation (group B). During the mean follow‐up duration of 20.5 ± 13.1 months, patients in group B showed significantly higher AF recurrence rates than those in group A after the ablation procedure (p = .017). Multivariate analysis revealed that DFT was the only predictive factor for AF recurrence (odds ratio, 1.07; 95% CI, 1.00–1.13, p = .047).ConclusionsThe DFT for IC was among the strongest prognostic factors in the peAF ablation procedure.

Defibrillation threshold modeling to refine implant recommendations for an extravascular ICD system

Abstract Background The extravascular ICD (EV ICD) is a novel defibrillator that couples a substernal lead to a device under the left axilla. The electrode locations for best defibrillation performance are unknown. In this study we use data from a 21 patient pilot study to address this question. Objective To create computational torso models to study the effect of device and lead position on defibrillation threshold (DFT). Methods Finite element models were developed from CT and intraoperative imaging of the 21 patients enrolled in the EV ICD Pilot Study. Between 150 and 200 combinations of electrode locations were created for each patient, including the actual implant locations as determined from post-implant CT. The shock amplitudes from DFT testing and multiple vector impedance measurements from a large subset of patients and their as-implanted models were used to calibrate global model parameters. In total, 3330 implant models were automatically meshed, simulated and analyzed to compute predicted DFT values. For each patient an acceptable implant zone was calculated in which it is predicted that they would pass implant DFT testing. The zones for all patients were aligned and combined using common anatomical landmarks so that a common zone for acceptable DFT performance could be calculated for the cohort. Results Two patients were omitted due to incomplete CT data and 16 models were used during the calibration phase. Final analysis was performed using 19 patient models. The model results recommend positioning the lead slightly left of the sternal midline with the most proximal electrode 10 mm above the xiphisternal junction. Similarly, the device should be positioned so that its upper margin is at the height of the leftmost projection of the heart as seen in the AP view, and its posterior margin aligned with the posterior margin of the ventricles. The figure illustrates these positions. The model predicts that using these locations will result in acceptable DFT performance for all 19 patients - including one who failed testing at implant. Conclusion Modeling showed that DFT is dependent on both lead and device location. Furthermore, the predicted DFT and impedance values are consistent with clinical measurements. Specific lead and device locations were determined that are both clinically identifiable and provide acceptable DFTs in all patients. Implant positioning Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Medtronic PLC

Implantation of looped epicardial cardioverter defibrillator coil on the surface of the right ventricular outflow tract.

We present the early results of looped epicardial cardioverter defibrillator coil implantation on the anterior surface of right ventricular outflow tract in infants and children. Patients with a surgical history of an epicardial implantable cardioverter defibrillator system between 2013 and 2014 were included in the study. Patient age, gender, body weight, indications for a cardioverter defibrillator system implantation, defibrillation threshold values, and defibrillation therapies were retrospectively evaluated. There were eight patients with a mean age of 4.4 ± 2.9 years and a mean body weight of 19.5 ± 11.7 kg. Five of the patients had been diagnosed with long QT syndrome, one patient had been diagnosed with genetic channelopathy and noncompaction of the left ventricle, and two patients had been diagnosed with univentricle physiology. The implantable cardioverter defibrillator system was composed of pace-sense leads, an abdominal active can, and a defibrillation coil placed below the pulmonary valve annulus on the anterior surface of the heart. The mean defibrillation threshold was 6.6 ± 2.3 joules. There were four appropriate therapies in two patients in a mean follow-up of 9 ± 6.5 months. The significantly low defibrillation thresholds with the defibrillation coils located below the pulmonary valve annulus are encouraging. However, a larger patient series will be necessary to evaluate the safety and reliability of this technique.

Subxiphoid Approach to Epicardial Implantation of Implantable Cardioverter Defibrillators in Children

Epicardial implantation of implantable cardioverter defibrillators (ICDs) is considered in the presence of intracardiac shunt, venous access issue, or small body size. We report our experience with epicardial ICD coil implantation using a minimally invasive method. Nine patients who underwent epicardial ICD implantation were included. The median age was 7.4 years (3.9-9.6 years) and the median weight was 15 kg (12-24 kg). Diagnosis at the time of implantation included long QT syndrome (n = 5), catecholaminergic polymorphic ventricular tachycardia (n = 2), hypertrophic cardiomyopathy (n = 1), and fast monomorphic ventricular tachycardia (n = 1). The minimally invasive method involved a subxiphoid incision to place the epicardial pacing leads. The ICD coil was placed in the transverse sinus in four patients using an access path posterior to the heart. The second approach involved a path anterior to the heart to reach the epicardial location posterior to the left atrial appendage in the five remaining patients. No fluoroscopy was used in either approach. The median defibrillation threshold (DFT) at implantation was 7.5 J. Lower DFTs were observed in the anterior approach (10 J vs 5 J). Appropriate ICD shocks were observed in three patients during the median 18-month follow-up period (0.3-28 months). No inappropriate shocks were noted. One patient developed pericardial tamponade 39 days after the procedure and was surgically drained. Minimally invasive epicardial ICD coil implantation in children with low DFT values is possible. The anterior implantation approach appears superior to the posterior approach.

Evaluation of shock waveform configuration on the defibrillation capacity of implantable cardioverter defibrillators in dogs

BackgroundImplantable cardioverter defibrillators (ICD) are programmed to detect ventricular arrhythmias and terminate them by delivering an electrical shock. A defibrillation threshold (DFT) at least 10 J below the maximum device output is recommended for successful therapy. Shock waveform configuration is a programmable parameter used to achieve a low DFT. It is hypothesized that a fixed-pulse configuration results in lower defibrillation energy requirements than a fixed-tilt configuration. Animals10 mongrel dogs. Materials and methodsICD generator and transvenous lead were surgically implanted. Defibrillation threshold was determined using a protocol guided by the upper limit of vulnerability. Fixed-pulse and fixed-tilt (50%/50%) waveform configurations were tested in a random order. Plasma cardiac troponin I (cTnI) was measured for signs of myocardial injury. ResultsThe experiment was completed in 9 dogs. Overall mean DFT value was 424 ± 88 V (9.2 ± 3.9 J). Mean differences among voltage, energy and impedance at the DFT for fixed-pulse (422 ± 97 V, 9.1 ± 4.2 J, 62.6 ± 13.8 Ω) and fixed-tilt (426 ± 83 V, 9.3 ± 3.8 J, 62.8 ± 18.5 Ω) configurations were not statistically significant (All P > 0.21). Cardiac TnI concentration changed from 0.03 ng/mL (95% CI: 0.02–0.04) at baseline to 0.11 ng/mL (95 CI: 0.08–0.16) after DFT was obtained with the first waveform configuration and 0.19 ng/mL (95% CI: 0.13–0.28) at the end of the study period. There were no significant changes in heart rate, end-tidal CO2 and blood pressure over time (all P > 0.09). ConclusionThe tested ICD device and lead placement reliably produced acceptable DFT values, based on a 10-J safety margin below the maximum device output. A benefit of fixed-pulse configuration could not be demonstrated over the standard fixed-tilt waveform. Signs of acute myocardial damage from repeated high-voltage shocks and episodes of ventricular fibrillation seemed of limited clinical significance.

Chronic Oral Amiodarone but not Dronedarone Therapy Increases Ventricular Defibrillation Threshold During Acute Myocardial Ischemia in a Closed-Chest Animal Model

Dronedarone, a recently approved antiarrhythmic drug, has been shown to have fewer side effects than amiodarone, particularly with regard to thyroid and neurologic events. Since the effects of either drug on ventricular defibrillation threshold during ischemia are unknown, the aim of this study was to compare the effects of dronedarone and amiodarone on defibrillation efficacy during ischemia in a closed-chest animal model. Dronedarone (30 mg·kg·d) and amiodarone (20 mg·kg·d) were administered orally for 3 weeks to 19 and 21 pigs, respectively. A control group (no treatment) comprised 19 pigs. A 2-lead endovascular defibrillation system was used. Each biphasic shock was delivered after 8 seconds of ventricular fibrillation. A step-up/step-down protocol was used to calculate mean defibrillation threshold before and 10 minutes after coronary artery occlusion using an angioplasty balloon in the left descending artery. At basal state, defibrillation threshold did not differ between the control (20.8 ± 4.8 J), amiodarone (21.2 ± 2 J), and dronedarone (19.5 ± 3 J) groups. After ischemia, the amiodarone group had a significantly higher defibrillation threshold than the control group (29.6 ± 3 J vs. 21.8 ± 5 J, respectively; P = 0.015), but the dronedarone (22.8 ± 4 J) and control groups had similar defibrillation threshold values. These data indicate that oral dronedarone treatment, unlike oral amiodarone, does not affect defibrillation threshold during ischemia in pigs.

Impact of Defibrillation Test Protocol and Test Repetition on the Probability of Meeting Implant Criteria

Defibrillation testing is a common procedure at defibrillator implant, with the purpose to ensure that each patient receives a device-lead system with a sufficient shock efficacy. The objective of this paper was to study the influence of defibrillation test protocols on the probability of passing implant testing. Defibrillation shock efficacy as a function of shock energy was modeled by a dose-response relationship estimated from the clinical data of the PainFREE Rx II study on 564 patients. A Monte Carlo method was used to simulate the outcomes of 12 commonly used defibrillation efficacy test protocols: four safety margin tests and eight protocols estimating the defibrillation threshold (DFT). The probabilities of failing 20-J and 25-J implant criteria for the different protocols ranged from 0.9% to 6.3% for 20 J and 0.3% to 3.4% for 25 J. Large variations in consecutively measured DFT values in the same patients were observed. Best results in the identification of “high risk” patients were obtained with the 2/2 safety margin protocol with an implant criterion of 20 J. The study also showed that the probability of patients inappropriately passing the implant criterion increased when the defibrillation test was repeated after initial failure. The defibrillation test protocol greatly influences the probability of meeting implant criterion. Therefore, these test protocols should be standardized. The model developed in this study, could be used to further understand their impact and to derive recommendations.

Effect of Substance Abuse on Defibrillation Threshold in Patients with Implantable Cardioverter‐Defibrillator

The use of recreational drugs has been observed to have deleterious effects on the heart. The aim of our study was to evaluate the effect of substance abuse on the defibrillation threshold (DFT) in patients with implantable cardioverter-defibrillators (ICDs). A retrospective analysis was conducted on patients who had undergone ICD placement at a tertiary university medical center in Detroit, Michigan. Subjects were identified based on self-reported drug use and placed into one of the three groups: controls, cocaine, and other illicit drugs. Due to a disparity in race among groups, the main analysis on DFT value was conducted on African-American patients only. Furthermore, exploratory analyses were conducted to investigate the effects of marijuana use and race on DFT values. A history of cocaine use (n = 17) significantly increases DFT among African Americans (17.3 ± 8 Joule [J] vs 12.5 ± 5 J in cases vs controls, P < 0.05), while previous use of marijuana does not significantly influence DFT. African-American patients with a history of illicit drug use had indications for ICD implantation at an earlier age and that within the control (nondrug using) group; African Americans (n = 73) had higher DFT compared to Caucasians (n = 32), (14.5 ± 0.5 J vs 9.7 ± 0.6 J, P < 0.05). A history of cocaine use in African Americans with ICD is a risk factor for high DFT and race itself (being African American) may be a risk for high DFT. Use of high-energy ICDs and other DFT lowering techniques may be considered for patients who have used or continue to use cocaine or in whom DFT testing cannot be performed at the time of implantation.

Do abandoned leads pose risk to implantable cardioverter-defibrillator patients?

With the increased number of implantable cardioverter-defibrillator (ICD) recipients and the frequent need for device upgrading, lead malfunction is a concern, but the optimal approach to managing nonfunctioning leads is unknown. The purpose of this study was to determine the rate and characteristics of complications related to abandoned ICD leads. Patients with abandoned leads were identified by retrospective review of the Mayo Clinic ICD database from August 1993 to May 2002. We reviewed the medical records to assess long-term follow-up for venous thromboembolic complications, device sensing malfunction, appropriateness of delivered shocks, defibrillation threshold (DFT) values before and after lead abandonment, and subsequent surgical procedures related to devices or leads. We identified 78 ICD patients (81% males; mean age 63 +/- 14 years) with 101 abandoned leads (69 in the right ventricle, 31 in the right atrium or superior vena cava, 1 in the coronary sinus). During a mean follow-up of 3.1 +/- 2.0 years, neither sensing malfunction nor venous thromboembolic complications were detected. DFT values were high in 13 patients (17%), but there was no significant increase in mean DFT values before and after lead abandonment in 43 patients for whom both values were available (16.2 +/- 9.2 J before abandonment vs 14.1 +/- 5.5 J after; P = .24). Fourteen patients (18%) required further ICD-related surgery; none of these operations were attributed to abandoned leads. Five-year rates of appropriate and inappropriate shocks were 25.9% and 20.5%, respectively. Abandoning a nonfunctioning lead appears to be safe and does not pose a clinically significant additional risk of future complications.

Effect of defibrillation testing on management during implantable cardioverter-defibrillator implantation

Verification of defibrillation efficacy by defibrillation threshold (DFT) testing during implantable cardioverter-defibrillator implantation is the current standard. Generally, defibrillation of ventricular fibrillation at 10 J below the maximum output of a device is felt to establish an adequate safety margin. Nonetheless, DFT testing adds to cost and carries some potential for morbidity, whereas its impact on outcomes in the modern era of defibrillator technology is unclear. We aimed to determine the frequency that DFT testing resulted in a change at device implant and to identify clinical and echocardiographic predictors of the need for DFT testing. We reviewed all implantable cardioverter-defibrillators that were implanted at the London Health Sciences Centre (Ontario, Canada) from June 1999 to August 2003 and used multivariate analysis to determine variables associated with DFT test failures and elevated DFT values. When a defibrillation failure was not observed, a lowest energy to defibrillate (LED) was recorded. Among 168 implants, DFT testing was successful with a minimum 10-J safety margin in 152 (90%), whereas the remaining 16 required changes at device implant. In a multivariate analysis, use of amiodarone was independently associated with DFT failure (odds ratio, 4.6; 95% confidence interval, 1.2-17.0). Significantly higher mean DFT/LED values were observed among patients on amiodarone (1.36 J; P = .0041). Those with nonischemic cardiomyopathy had a higher mean DFT/LED compared with those with ischemic cardiomyopathy (1.44 J; P = .028). Use of amiodarone is associated with a 4-fold increase in risk of DFT failure and subsequent need for changes at implant to achieve a safe threshold. Defibrillation threshold testing appears to be most useful for patients taking amiodarone.

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.

Hypertonic saline does not reverse the sodium channel blocking actions of lidocaine: evidence from electrophysiologic and defibrillation studies.

Studies have shown that increasing extracellular sodium concentration can partially reverse sodium channel blockade. However, there is conflicting in vitro evidence in this regard for lidocaine. The effects of lidocaine on cardiac electrophysiology and defibrillation were studied in a basal and hypernatremic state to determine reversibility of sodium channel blockade. Electrophysiologic studies measured right ventricular effective refractory period at 350 ms pacing cycle length and QRS interval, JT interval, and monophasic action potential duration during sinus rhythm and right ventricular pacing (350 ms cycle length) in 14 pentobarbital-anesthetized swine (25-30 kg). Defibrillation threshold (DFT) was measured by quantitating successful conversion of sustained ventricular fibrillation to normal sinus rhythm. Each pig was randomly assigned to a treatment group with three study phases; group 1 = baseline, lidocaine (20 mg/kg/h), and lidocaine plus placebo (D5W; n = 7); and group 2 = baseline, lidocaine, and lidocaine plus hypertonic saline (2-3 mM/kg/h; n = 7). In groups 1 and 2, lidocaine infused alone significantly (p < 0.01) increased DFT values from baseline (9.8 +/- 3.9 to 15.7 +/- 5.8 J and 8.9 +/- 2.9 to 14.7 +/- 5.4 J, respectively) and increased QRS duration from baseline during right ventricular pacing (89 +/- 6 to 109 +/- 10 ms; p < 0.01; and 87 +/- 6 to 103 +/- 12 ms; p < 0.01). Lidocaine alone reduced right ventricular action potential duration (APD) in groups 1 and 2 (214 +/- 18 to 206 +/- 20 ms; p < 0.10; and 228 +/- 8 to 212 +/- 8 ms; p < 0.05), respectively, and it reduced paced JT interval in both groups (194 +/- 20 to 184 +/- 18 ms; p < 0.10; and 200 +/- 12 to 183 +/- 16 ms; p < 0.05), respectively. When hypertonic saline was added to lidocaine, DFT and QRS duration values were unaffected (14.7 +/- 5.4 to 16.1 +/- 3.7 J and 103 +/- 12 to 100 +/- 11 ms, respectively). However, APD and JT intervals returned to basal values when hypertonic saline was added to lidocaine (212 +/- 8 to 225 +/- 13; p < 0.05; and 183 +/- 16 to 192 +/- 18; p < 0.05, respectively). When D5W was added in the control group, no changes occurred in DFT or electrophysiologic values. Lidocaine slowed ventricular conduction velocity and reduced APD. The administration of hypertonic saline to increase extracellular sodium concentrations failed to reverse the effect of lidocaine on conduction-velocity slowing or elevated DFT values. Hypertonic saline did reverse the effects of lidocaine on repolarization parameters. These data suggest that shortening of repolarization is not a mechanism by which lidocaine makes it more difficult to defibrillate the heart.

Influence of Hypertonic Saline Solution Infusion on Defibrillation Efficacy

Hypertonic saline solution may enhance cardiac conduction via the fast inward sodium channel and alter transmembrane Ca+2 conductance via the sodium-calcium exchanger. Evidence suggests that both Ca+2 conductance and myocardial conduction velocity may affect ventricular defibrillation. Since hypertonic saline solution solutions (ie, sodium bicarbonate) may be administered to patients who have conditions that often require ventricular defibrillation (ie, cardiac arrest or hypovolemic shock), we studied the effect of hypertonic saline solution on the defibrillation threshold (DFT) in 16 pentobarbital-anesthetized domestic farm swine (20 to 30 kg). Defibrillation was performed using two interfaced epicardial electrode patches. DFTs were determined at baseline and during treatment phase. Pigs were randomly assigned to treatment consisting of either hypertonic saline solution (6 mmol/kg load, 2.0 to 3.0 mmol/kg infusion) to maintain serum sodium concentrations 10 to 15 mmol/L above baseline or control (D5W given in equal volume). DFT values (joules) that predicted 50% success were modeled from a best-fit histogram. Hypertonic saline solution did not change DFT values from baseline values (10.2 +/- 4.3 vs 10.8 +/- 7.0, respectively). Likewise, placebo (D5W) did not change DFT values from baseline values (10.1 +/- 4.5 vs 11.3 +/- 4.3). During treatment phase, DFT values were 99 +/- 28% of baseline values in the hypertonic saline solution group and 116 +/- 23% of baseline values in the D5W groups (p = 0.21). The administration of hypertonic saline solution also did not affect ventricular conduction velocity, right ventricular action potential duration, or right ventricular effective refractory period. These data indicate that hypertonic saline solution does not appreciably affect defibrillation efficacy or electrical treatment of ventricular fibrillation.

Mechanisms of antiarrhythmic drug-induced changes in defibrillation threshold: Role of potassium and sodium channel conductance

Objectives.We sought to determine which ion current predominantly affects defibrillation outcomes by using specific pharmacologic probes (lidocaine [a sodium channel blocking agent] and cesium [an outward potassium channel blocking agent]) in 26 swine.Background.The effect of a drug on sodium or potassium channel conductance, or both, may affect defibrillation threshold values. However, it is unknown which ion channel predominates.Methods.Each pig was randomly assigned to one of four treatment groups with two treatment phases: groupI = placebo (D5W) in treatment phase I followed by placebo plus cesium in treatment phase II (n = 6); group 2= lidocaine followed by lidocaine plus placebo (n = 7); group 3= lidocaine followed by lidocaine plus cesium (n = 7); group 4= placebo followed by placebo plus placebo (n = 6). Defibrillation threshold values and electrocardiographic measurements were obtained at baseline and at treatment phases I and II.Results.Lidocaine increased defibrillation threshold values from baseline by 71% in group 2 (p = 0.02) and by 92% in group 3 (p < 0.01). There were no changes in defibrillation threshold values from baseline to D5W in groups 1 and 4. When D5W was added to lidocaine in group 2 and D5W in group 4, there were no significant changes in defibrillation threshold values. However, when cesium was added to lidocaine in group 3, the elevated defibrillation threshold values (mean ± SD) returned to baseline values (from 15.7 ± 3.46 to 7.55 ± 3.19 J, p < 0.01). Cesium added to D5W in group 1 also significantly reduced defibrillation threshold values from 7.10 ± 1.27 to 4.14 ± 1.75 J (p < 0.01). The effect of cesium on defibrillation threshold values was similar between groups 1 and 3, regardless of lidocaine, such that these values were reduced by 40 ± 14% and 51 ± 18%, respectively (p = 0.28).Conclusions.Cesium, through potassium blockade, reverses lidocaine-induced elevation in defibrillation threshold values. The magnitude of defibrillation threshold reduction when cesium was added to lidocaine was similar to the defibrillation threshold reduction when cesium was added to placebo. Thus, inhibiting outward potassium conductance and prolonging repolarization decreases defibrillation threshold values independent of sodium channel blockade.

Differential effects of lidocaine on defibrillation threshold with monophasic versus biphasic shock waveforms.

Defibrillation waveforms and antiarrhythmic drugs have disparate effects on myocardial excitability and refractoriness, making it likely that antiarrhythmic drugs will interact with one waveform differently than with another. The aim of the present study was to determine if the increase in defibrillation threshold (DFT) induced by lidocaine is similar for electrical shocks with monophasic and biphasic waveforms. Twenty-six pentobarbital-anesthetized farm-raised pigs were instrumented with pacing catheters and epicardial defibrillation electrodes. Each pig was assigned to one of four groups: (1) monophasic shock waveform and placebo (5% dextrose in water [D5W]) (n = 7), (2) monophasic shock waveform and lidocaine (n = 7), (3) biphasic shock waveform and placebo (D5W) (n = 5), or (4) biphasic shock waveform and lidocaine (n = 7). DFT was measured at baseline and subsequently during treatment (D5W or lidocaine). In the monophasic waveform groups, DFT increased from baseline in response to lidocaine by 92% (P < .0001), whereas DFT values in response to D5W did not change. In the biphasic waveform groups, DFT values did not change from baseline in response to lidocaine (P = NS), whereas DFT values from baseline in response to D5W significantly decreased by 29% (P = .04). In the monophasic waveform groups, the change in DFT from baseline in response to lidocaine was significantly different than the change from baseline in response to D5W (92 +/- 29% versus -0.5 +/- 29%, respectively) (P < .0002). In the biphasic waveform groups, however, the change in DFT from baseline in response to lidocaine was similar to the change from baseline in response to D5W (-5.66 +/- 15% versus -29 +/- 17%, respectively) (P = .48). Furthermore, the change in DFT from baseline in response to lidocaine differed significantly between monophasic and biphasic waveform groups (92 +/- 29% versus -5.66 +/- 15%) (P < .0002), whereas the change from baseline in response to D5W did not differ between monophasic and biphasic waveforms (-0.5 +/- 29% versus -29 +/- 17%) (P = .34). Compared with placebo groups, DFT values increased during lidocaine treatment to a much greater degree in the monophasic waveform group than in the biphasic waveform group receiving lidocaine. These data support our hypothesis that antiarrhythmic drugs can affect the defibrillation efficacy of monophasic waveforms differently than that of biphasic waveforms.

767-5 Differential Effects of Lidocaine on Defibrillation Threshold with Monophasic and Biphasic Waveforms

Antiarrhythmic drugs can interfere with electrical defibrillation using monophasic non-sequential shocks (MS). It is unknown if these drugs affect the efficacy of biphasic defibrillation shocks (BS). Since MS and BS waveforms can exhibit disparate effects on myocardial excitability and refractoriness (properties which may influence defibrillation efficacy), it is possible that antiarrhythmic drugs, such as lidocaine (L), will affect defibrillation threshold (DFT) of one waveform differently than another. We studied 25 pentobarbital anesthetized farm swine who had endocardial pacing and monophasic action potential catheters placed into the right ventricle. Pacing was used to induced sustained ventricular fibrillation (5-8 s) which was followed by defibrillation via epicardial electrodes. Each pig was assigned to one of four treatment groups; 1) MS + D5W (n = 7), 2) MS + L (n = 7) 3) BS + D5W (n = 5), or 4) BS + L (n = 7). DFTs were measured at baseline (Base) and subsequently during treatment (D5W or L). DFT values (joules) predicting 50% success at baseline were: + D5W = 7.34 ± 1.59, MS + L= 7.11 ± 1.5, BS + D5W = 5.28 ± 1.55 and BS + L = 3.86 ± 1.2. The figure depictsDownload : Download high-res image (130KB)Download : Download full-size imagetreatment DFT values as percent of baseline. In the MS groups, the change in DFT from Base to L was 92 ± 28% vs the change from Base to D5W of 0.6 ± 29% (p &lt; 0.0001). In the BS groups, however, the change in DFT from Base to L was similar to the change from Base to D5W (-6.7 ± 15 vs -29 ± 17%, p = 0.08). Compared to D5W, L increased DFT in the biphasic group by a magnitude that was ¼ that seen in the monophasic group. Clinical Implications: The effect of antiarrhythmic drugs on DFT (especially increased DFT values) may be less of a concern when using implantable devices employing biphasic waveforms.

767-3 Reverse Polarity Biphasic Defibrillation with Three Biphasic Waveforms Using a Unipolar Defibrillation System

In ten dogs we assessed the impact on defibrillation success of reverse polarity biphasic shocks, using the CPI, Medtronic and Ventritex biphasic waveforms delivered through a right ventricular (RV) coil/CAN system. In each animal the three biphasic waveforms were tested in random order. Similarly with each waveform the defibrillation threshold (DFT) achieved using the standard and reverse polarity were randomly determined. A 5 cm long coil with 426 mm2 surface area was advanced in the RV through the jugular vein and the 80 cm2 defibrillator can was placed in the subcutaneous tissue of the left superior chest wall. Shocks were delivered between the RV coil as cathode and the CAN as anode (standard polarity) and vice versa (reverse polarity). Triplicate defibrillation thresholds were obtained with each biphasic waveform. DFT values are shown below:Empty CellCPIMedtronicVentritexDFT Standard (J)70 ± 2.28.3 ± 3.593 ± 4.3DFT Reverse (J)4.6 ± 1.25.2 ± 2.56.7 ± 3.7CPI Standard vs Reverse p &lt; 0.01; Medtronic Standard vs Reverse p &lt; 0.01; Ventritex Standard vs Reverse p &lt; 001 CPI Standard vs Reverse p &lt; 0.01; Medtronic Standard vs Reverse p &lt; 0.01; Ventritex Standard vs Reverse p &lt; 001 When defibrillation shocks are delivered through a single right ventricular lead/defibrillator can system reverse polarity provides better defibrillation efficacy regardless of the biphasic waveform used.