Seconds Of Ventricular Fibrillation Research Articles

Abstract 13358: Pediatric Defibrillation; Safety and Efficacy of Shocks in Both Ventricular Fibrillation and Sinus Rhythm in a Porcine Model

Introduction: Pediatric sudden cardiac arrest may require the delivery of a defibrillating shock to promote return of spontaneous circulation (ROSC). Fear of harm is a barrier for the use of automated external defibrillators by lay personnel, particularly when the patient is a child. The aim of this study was to observe the effects of delivering pediatric defibrillation shocks to pediatric weight swine who are in a perfusing rhythm or ventricular fibrillation (VF). Methods: Eight swine (10.3-26.8 kg) were studied under anesthesia. Up to 30 shocks were applied using modified samaritan AEDs (HeartSine, UK) to animals either in sinus rhythm or after 30 seconds of VF. Shocks delivered in sinus rhythm were unsynchronized. Four different shock types were applied, utilizing two different waveforms (Waveform-A at 50 J, Waveform-A at 75 J, Waveform-A at 90J and Waveform-B at 50 J). Left ventricular (LV) pressures were recorded invasively (Millar, USA). If the shock was successful, the animal entered a rest period of approximately 5 minutes, after which the next shock was applied. Results: Data presented in Table 1. Out of a total of 77 shocks delivered in sinus rhythm, 2 (2.6%) resulted in conversion to a cardiac arrest rhythm. Analysis of LV pressures demonstrated no significant differences in the change of LV dP/dt from baseline at 1, 10 and 60 seconds post-shock. There was no significant difference in shock success or ROSC between the shock types for defibrillation of VF. Analysis of LV pressures demonstrated no significant differences in the change of LV dP/dt from baseline at at 1, 10 and 60 seconds post-shock between the groups. Conclusions: The results of this study indicate defibrillation shocks applied to swine in sinus rhythm rarely result in conversion to an arrhythmia. Additionally, the variety of shock types demonstrated similar levels of safety and efficacy in this porcine model.

Radiofrequency ablation in Brugada syndrome.

Radiofrequency ablation in Brugada syndrome.

"Vasovagal" response during ventricular fibrillation: incidence and implications.

The purpose of this study was to assess the relationship between changes in sinus node cycle length (SNCL) during ventricular fibrillation (VF) and the peripheral changes in blood pressure (BP) and sympathetic nerve activity (SNA) in human subjects. We hypothesized that patients with no SNCL shortening during VF have a vasovagal-like response with a greater decrease in BP and SNA when compared to patients with SNCL shortening. SNCL, BP, and SNA recordings were attempted in 24 patients undergoing the implantation of a dual-chamber implantable defibrillator. Changes were measured during the first 5 seconds of VF and compared with the 5 seconds prior to VF induction. SNCL shortened during VF in nine patients (mean%∆SNCL = -12 ± 8%) and remained unchanged or lengthened in seven patients (mean%∆SNCL = 7 ± 7%). Eight patients had ventriculoatrial (VA) conduction prohibiting assessment of SNCL changes. In patients with SNCL shortening, the %∆MBP (mean BP) was -47 ± 6% compared to -58 ± 8% in patients with no SNCL shortening (P < 0.01). In patients with VA conduction, the %∆MBP was -54 ± 3%. SNA recordings were successfully obtained in four patients. When compared to baseline, SNA increased by 34 ± 30% in two patients with SNCL shortening, decreased by 25% in one patient with SNCL lengthening, and by 90% in the fourth patient with VA conduction. We have shown that patients with no SNCL shortening have a significantly greater decrease in MBP during VF when compared to patients with SNCL shortening. The underlying mechanism appears to be reflex mediated with a vasovagal-like response in patients with no SNCL shortening.

Ascending-Ramp Biphasic Waveform Has a Lower Defibrillation Threshold and Releases Less Troponin I Than a Truncated Exponential Biphasic Waveform

We tested the hypothesis that the shape of the shock waveform affects not only the defibrillation threshold but also the amount of cardiac damage. Defibrillation thresholds were determined for 11 waveforms-3 ascending-ramp waveforms, 3 descending-ramp waveforms, 3 rectilinear first-phase biphasic waveforms, a Gurvich waveform, and a truncated exponential biphasic waveform-in 6 pigs with electrodes in the right ventricular apex and superior vena cava. The ascending, descending, and rectilinear waveforms had 4-, 8-, and 16-millisecond first phases and a 3.5-millisecond rectilinear second phase that was half the voltage of the first phase. The exponential biphasic waveform had a 60% first-phase and a 50% second-phase tilt. In a second study, we attempted to defibrillate after 10 seconds of ventricular fibrillation with a single ≈30-J shock (6 pigs successfully defibrillated with 8-millisecond ascending, 8-millisecond rectilinear, and truncated exponential biphasic waveforms). Troponin I blood levels were determined before and 2 to 10 hours after the shock. The lowest-energy defibrillation threshold was for the 8-milliseconds ascending ramp (14.6±7.3 J [mean±SD]), which was significantly less than for the truncated exponential (19.6±6.3 J). Six hours after shock, troponin I was significantly less for the ascending-ramp waveform (0.80±0.54 ng/mL) than for the truncated exponential (1.92±0.47 ng/mL) or the rectilinear waveform (1.17±0.45 ng/mL). The ascending ramp has a significantly lower defibrillation threshold and at ≈30 J causes 58% less troponin I release than the truncated exponential biphasic shock. Therefore, the shock waveform affects both the defibrillation threshold and the amount of cardiac damage.

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.

Panoramic optical mapping shows wavebreak at a consistent anatomical site at the onset of ventricular fibrillation

The first seconds of ventricular fibrillation (VF) are well organized and can consist of just one to two rotating waves (rotors). New rotors are spawned when local propagation block causes wave fragmentation. We hypothesized that this process, which leads to fully developed VF, begins at a consistent anatomic site. We initiated VF with a stimulus timed to the local T-wave in 10 isolated pig hearts. Hearts were stained with a voltage-sensitive dye and four video cameras recorded electrical propagation panoramically across the epicardium. In each VF episode, we identified the position of the first wavebreak event that produced new rotor(s) that persisted for at least one cycle. The first such wavebreak occurred along the anterior right ventricular insertion (ARVI) in 26 of 32 VF episodes. In these episodes, wavebreak sites were 6 ± 4 mm from the midline of the ARVI. In the remaining 6 episodes, wavebreak sites were 24 ± 5 mm from the midline on either the LV or RV. During rapid pacing, conduction speed was locally depressed at the ARVI when waves crossed parallel to the midline. Action potential duration (APD) was slightly longer (2.2 ± 2.1 ms) at the ARVI compared with other sites (P< 0.01). Temporal APD alternans were small and not unique to the break site, suggesting that dynamic APD properties were not the cause of wavebreak. The ARVI is the dominant site for wavebreak at the onset of VF in normal myocardium. This may be due to the anatomic complexity of the region.

Abstract 274: Filter Out the Chest Compression Signal Interference During Ventricular Fibrillation by Signal Processing

Background: Ventricular fibrillation (VF) is the major cause of sudden cardiac death. The most effective way to stop VF is to defibrillate. However, current automated external defibrillator does not allow chest compression when doing electrogram analysis. Many studies have shown that the mortality rate of VF increased rapidly when the “hands-off” intervals lengthen. The goal of the present project is to develop a new method to filter the chest compression signals in ECG and to reduce the “hands-off” time. Methods: We induced VF in rat and the precordial compression was performed with a pneumatically driven mechanical chest compressor at different frequency (150cpm, 200cpm, 300cpm) for 30 seconds after 30 seconds of VF. The ECG signals were processed with empirical mode decomposition and comb filter to filter out the chest compression signals. We then calculated the spectrogram to prove the effect of the filter and the amplitude spectrum analysis (AMSA) to demonstrate the time evolution of VF during and after chest compression. Results: A total of 6 rats in each group were studied. From the spectrogram, we found that the chest compression signals were effectively removed after signal processing. Moreover, the AMSA significantly increased in VF group with chest compression at rate 150cpm. When stopping chest compression, the AMSA rapidly decreased in all groups. Conclusions: The chest compressions signals in ECG can be effectively filtered out from VF by the combination of EMD and comb filter.

264 Is ventricular fibrillation different in ischemic compared to non-ischemic dilated cardiomyopathic human hearts?

It is unknown if VF dynamics are dependent on the etiology of the cardiomyopthay. In this study we compared transmural dominant frequency gradient, during ventricular fibrillation (VF), in ischemic and non-ischemic dilated cardiomyopathic human hearts. The study was conducted in human langendorff model. These were ischemic (ICM, n = 5) and dilated (DCM, n = 5) cardiomyopathic human hearts explanted from patients undergoing cardiac transplant. Data was collected using an epicardial sock and an endocardial balloon each having 112 unipolar electrodes, arranged in 14 columns and 8 rows. Ischemia was induced by halting the perfusion to the heart and VF was initiated by brief application of 9V batter to epicardium. VF was recorded at onset, 90 seconds and 180 seconds for 20 seconds each. Dominant frequency (DF) was computed using Welch periodogram method as described in our previous studies. Repeated measure ANOVA was employed using mixed model in SAS. The mean DF in LV-endocardium and LV-epicardium is reported in table 1. At the onset of VF, no difference was observed between LV epicardium and endocardium in dilated cardiomyopathic hearts (P = 0.6) while the difference was statistically significant in ischemic cardiomyopathic hearts (P < 0.05). After 180 seconds of VF, there was a significant transmural DF gradient in both ischemic and dilated cardiomyopathic hearts (P < 0.05).Tabled 1 There is a LV transmural DF gradient during VF in both DCM and ICM after 3 minutes of ischemia. This gradient is established early in ischemia in ICM but not in DCM. These finding may relate to differential transmural ion channel remodelling that is dependent of the etiology of cardiomyopathic process.

Coronary Blood Flow Produced by Muscle Contractions Induced by Intracardiac Electrical CPR during Ventricular Fibrillation

It has been reported that transthoracic electrical cardiopulmonary resuscitation (ECPR) generates coronary perfusion pressures (CPP) similar to manual chest compressions (MCC). We hypothesized that intracardiac ECPR produces similar CPP. ECPR pulse train protocols were applied for 20 seconds in a porcine model following 10 seconds of ventricular fibrillation (VF), using a defibrillator housing electrode and a right ventricular coil (IC-ECPR). Each protocol consisted of 200-ms electrical pulse trains applied at a rate of 100 pulse trains/min. The protocols were grouped in skeletal-based versus cardiac-based stimulation measurements. CPP was recorded and compared to historical MCC values generated by a similar experimental design. CPP > 15 mm Hg at 30 seconds of VF following the application of an IC-ECPR protocol was defined as successful. Mean CPP for all intracardiac ECPR pulse train protocols at 30 seconds of VF was 14.8 +/- 3.8 mm Hg (n = 39). Mean CPP in seven successful skeletal-based IC-ECPR protocols was 19.4 +/- 3.2 mm Hg, and mean CPP in 10 successful cardiac-based IC-ECPR protocols was 17.4 +/- 2.1 mm Hg. Reported CPP for 15 MCC experiments at 30 seconds of VF was 22.9 +/- 9.4 mm Hg (P = 0.35 compared to skeletal-based IC-ECPR, P = 0.08 compared to cardiac-based IC-ECPR). Intracardiac applied electrical CPR produced observable skeletal muscle contractions, measurable pressure pulses, and coronary perfusion pressures similar to MCC during a brief episode of untreated VF.

The Long and the Short of Long and Short Duration Ventricular Fibrillation

See related article, pages 1256–1264 The mechanisms behind the complex activation sequences during ventricular fibrillation (VF) have been the topic of intense research over many years. Experimental studies in animal models of VF, as well as clinical studies of human VF,1–8 have provided a wealth of data on the nature of electric activity in the fibrillating heart. Supplemented by computer simulations and a theoretical framework of wave propagation in excitable media,9,10 our community has amassed significant insights into the mechanisms that lead to the degradation of electric activity into VF and of VF maintenance. However, the majority of these studies have been devoted to VF mechanisms in the short time period after VF onset (short-duration VF, lasting less than 1 minute). In an episode of cardiac arrest outside of the hospital, the median time to delivery of the first defibrillation shock is 4.4 minutes,11 with VF episodes often lasting as long as 10 minutes (long-duration VF); over this period, the heart becomes ischemic while being subjected to excessively high excitation rates. Changes in the electrophysiological properties of the myocardium take place over these long-duration VF episodes. This is reflected in the altered outcome of a defibrillation shock, with survival rates decreasing rapidly with the increase in minutes spent in VF.12 Similarly, the guidelines for optimal resuscitation therapy differ depending on VF duration: immediate defibrillation is prescribed if time from VF onset is less than 4 or …

The Impact of Acute Myocardial Ischemia on the Ventricular Defibrillation Threshold During Chronic Oral Azimilide Therapy

The effects of chronic oral azimilide therapy on the ventricular defibrillation threshold (DFT) during ischemia are unknown. The effects of azimilide on defibrillation efficacy under ischemic condition were investigated in a closed-chest animal model. Azimilide (20 mg/kg/d) was administered orally for 7 days to 10 pigs (20 to 25 kg). The control group (no treatment) comprised 15 pigs. A 2-lead defibrillation system was used. Each shock was delivered after 8 seconds of ventricular fibrillation. A step-up and step-down protocol was used to calculate mean DFT before and 10 minutes after coronary artery occlusion using an angioplasty balloon in the left descending artery. The basal DFT of the azimilide group did not differ from controls (20.8 +/- 4.8 versus 18.8 +/- 2.8; P = 0.33). After ischemia, the mean DFT of the azimilide-treated animals was similar to controls (21.8 +/- 5.2 versus 23.2 +/- 3.8 J; P = 0.54), despite significant lengthening of ventricular repolarisation (428.2 +/- 51.8 versus 494.1 +/- 46.6 msec; P = 0.005) and significant prolongation of the ventricular fibrillation cycle length (85.1 +/- 13 versus 104.7 +/- 24 msec; P < 0.04). Chronic oral azimilide treatment does not affect the DFT at baseline or during acute myocardial ischemia.

Heterogeneity of Ventricular Fibrillation Dominant Frequency During Global Ischemia in Isolated Rabbit Hearts

Ventricular fibrillation (VF) studies show that ECG-dominant frequency (DF) decreases as ischemia develops. This study investigates the contribution of the principle ischemic metabolic components to this decline. Rabbit hearts were Langendorff-perfused at 40 mL/min with Tyrode's solution and loaded with RH237. Epicardial optical action potentials were recorded with a photodiode array (256 sites, 15 x 15 mm). After 60 seconds of VF (induced by burst pacing), global ischemia was produced by low flow (6 mL/min), or the solution changed to impose hypoxia (95% N2/5% CO2), low pH(o) (6.7, 80% O2/20% CO2), or raised [K+](o) (8 mM). DF of the optical signals was determined at each site. Conduction velocity (CV), action potential duration (APD90), effective refractory period (ERP), activation threshold, dV/dt(max), and membrane potential were measured in separate experiments during ventricular pacing. During VF, ischemia decreased DF in the left ventricle (LV) (to [58 +/- 6]%, P < 0.001), but not the right (RV) ([93 +/- 5]%). Raised [K+](o) reproduced this DF pattern (LV: [67 +/- 12]%, P < 0.001; RV: [95 +/- 9]%). LV DF remained elevated in hypoxia or low pH(o). During ventricular pacing, ischemia decreased CV in LV but not RV. Raised [K+](o) did not change CV in either ventricle. Ischemia and raised [K+](o) shortened APD90 without altering ERP. LV activation threshold increased in both ischemia and raised [K+](o) and was associated with diastolic depolarization and decreased dV/dt(max). These results suggest that during VF, decreased ECG DF in global ischemia is largely due to elevated [K+](o) affecting the activation thresholds in the LV rather than RV.

Effects of Sildenafil Citrate on Defibrillation Efficacy

Although fatal arrhythmia and sudden death have been reported in patients taking sildenafil citrate, its effect on defibrillation efficacy has not been investigated. The aim of this study was to test the hypothesis that sildenafil citrate increases the shock strength required to successfully defibrillate during ventricular fibrillation (VF). A total of 26 pigs (20-25 kg) were randomly assigned into three groups. In each group, the defibrillation threshold (DFT) was determined at the beginning of the study using a three-reversal up/down protocol. Each shock (RV-SVC, biphasic) was delivered after 10 seconds of VF. Group 1 (n = 10) received 50 mg and group 2 (n = 10) received 100 mg of sildenafil citrate intravenously at a rate of 2 mL/minute for 50 minutes. Group 3 (n = 6) received 100 mL of saline intravenously at the same rate as in group 1. The DFT was determined again after the drug (drug-DFT) and saline (saline-DFT) administration. For 100-mg sildenafil citrate infusion, the DFT (483 +/- 39 V, 18 +/- 3 J) was significantly (P < 0.003 and P < 0.01, respectively) higher than the control-DFT (407 +/- 123 V, 13 +/- 7 J). This sildenafil citrate infusion increased the DFT approximately 19% by voltage, and approximately 38% by total energy. After 50-mg sildenafil citrate infusion, the DFT (454 +/- 28 V, 15 +/- 2 J) was not different than the control DFT (449 +/- 28 V, 15 +/- 2 J). Saline infusion (391 +/- 18 V, 12 +/- 1 J) did not alter the control DFT (399 +/- 22 V, 12 +/- 1 J). The 100-mg sildenafil citrate infusion, representing a supra-therapeutic plasma level, significantly increased the DFT. This finding indicates that VF occurring during supra-therapeutic sildenafil citrate treatment would require a stronger shock to successfully defibrillate.

Quantification of activation patterns during ventricular fibrillation in open-chest porcine left ventricle and septum

A single stationary mother rotor has been hypothesized to be responsible for maintenance of ventricular fibrillation (VF) in the guinea pig. Previous studies have pointed to the ventricular septum as a possible location for a mother rotor in the pig heart. The purpose of this study was to test the hypothesis that a mother rotor is located in the septum. In seven open-chest pigs, we mapped the first 20 seconds of electrically induced VF simultaneously from the posterior left ventricle (LV) and right side of the septum with two electrical arrays. Each array contained 504 electrodes (21 x 24) spaced 2 mm apart in the LV and 1.5 mm apart in the septum. The percentage of VF wavefronts that formed reentrant circuits was significantly lower in the septum (1% +/- 1% [mean +/- SD]) than in the LV (2% +/- 1%). The peak frequency during VF also was significantly smaller in the septum (8.6 Hz +/- 3.0 Hz) than in the LV (10.4 Hz +/- 3.4 Hz). The mean direction of spread of activation of VF wavefronts was away from the region where the posterior LV free wall intersects the posterior septum in both the LV and septum. The lower incidence of reentry and lower peak frequency in the mapped region of the septum than in the LV indicate that a mother rotor is not present in swine on the RV side of the septum. The mean directions of the VF activation sequences in the LV and septum suggest that if a mother rotor is present during the first 20 seconds of VF, it exists where the posterior LV free wall joins the septum, the region where the posterior papillary muscle inserts.

The duration of ventricular fibrillation required to produce pulseless electrical activity

The duration of untreated (no cardiopulmonary resuscitation) ventricular fibrillation (VF) needed to produce postdefibrillation pulseless electrical activity (PEA) was determined in 9 anesthetized swine ranging in weight from 20 to 30 kg. VF was induced electrically by a right ventricular catheter electrode, while arterial pressure and the electrocardiogram were recorded. VF was confirmed by the presence of VF waves in the electrocardiogram and a loss of pulsatile arterial pressure. VF was allowed to persist for 15-second increments (eg, 15, 30, 45, etc), after which defibrillation was achieved with transchest electrodes and the presence or absence of PEA was noted. If PEA was present, rhythmic chest compressions were applied to rescue the animal. Just after initiation of VF and just before defibrillation, VF wave frequency was measured. PEA was encountered in 100% of the trials after 180 seconds of VF. The threshold duration for PEA was 60 seconds. VF wave frequency decreased with the passage of time. At VF initiation, VF wave frequency ( f 0) ranged from 6 to 15 per second, with a mean of 10.1 ± 2.1 per second. At 180 seconds ( f 180), the mean frequency was 4.0 ± 0 per second. It was only possible to eliminate PEA and restore pumping in 1 animal when untreated VF lasted more than 180 seconds. There was no clear transition in the frequency of the VF waves with the passage of time that could predict the possibility of postdefibrillation PEA. Moreover, because of the different initial VF wave frequencies and the different rates of decrease with time, a measurement of VF wave frequency is unlikely to be informative on how long VF had been present. A consistent finding in this swine study of prolonged untreated VF was a rise in blood K + which increased from a normal prefibrillation value of about 4 mEq/L to 8 to 12 mEq/L at 180 seconds. The longer the duration of VF, the higher the K +.

Systematic evaluation of the determinants of defibrillation efficacy

We studied the effect of varying shock capacitance, shock impedance, and pulse duration on defibrillation efficacy in a randomized, crossover manner for biphasic shocks. The relationship between the electrical determinants of defibrillation efficacy is incompletely understood. Biphasic shocks were delivered to 12 dogs through epicardial patches (to vary impedance) after 15 seconds of ventricular fibrillation using one of 100- or 155-muF capacitors at each of four pulse durations (2.5, 5, 10, 20 ms), in a balanced random order. There were two impedance groups: six with higher impedance (mean 97 +/- 15 Omega, range 80-120) and six with lower impedance (mean 39 +/- 3 Omega, range 34-44). Voltage requirements were estimated as the average of three defibrillation threshold (DFT) tests. Shock capacitance, resistance, and pulse duration all had significant effects upon the minimum voltage DFT (P = .0065, P = .0066, and P = .0001, respectively). The tilt associated with the lowest voltage and current requirement for each of the four capacitance/resistance combinations varied widely, between 34 +/- 5% and 63 +/- 3%, depending on capacitance and impedance. The optimal pulse duration associated with minimum DFT lies between 5.11 and 5.34 ms. Defibrillation voltage requirements for biphasic shocks are affected by pulse duration, capacitance and impedance, but not "tilt."

Restitution Properties During Ventricular Fibrillation in the In Situ Swine Heart

Although restitution has been hypothesized to determine action potential duration (APD) during ventricular fibrillation (VF), cardiac memory may also be important. Transmembrane recordings were made with a floating microelectrode from the anterior right ventricular wall in 6 pigs during up to 60 seconds of VF. The recordings were divided into 5-second intervals, and APD60 and the diastolic interval (DI) were calculated for each activation cycle throughout each interval. Stepwise linear regression was used to determine how well each APD60 [APD60(n)] was predicted by the 4 previous DIs (n-1, n-2, n-3, n-4) and the 3 previous APD60s (n-1, n-2, n-3). A mean+/-SD of 3+/-1.5 of the variables entered the regression equation. DI(n-1) (70% of intervals) and APD60(n-1) (71% of intervals) appeared most frequently in the regression equations and were the first or second variables entered during the stepwise regression in 87% and 76% of the intervals in which they were present, respectively. The coefficients of DI(n-1) and APD60(n-1) were positive 89% and 98% of the time, respectively. R2 of the regression for all entered variables during all intervals was 0.39+/-0.05. The high incidence and positive coefficient of DI(n-1) indicate that restitution is important in determining APD during VF, whereas the similarly high incidence and positive coefficient of APD(n-1) indicate that cardiac memory is equally important. The finding that the regression equation accounts for only 39% of the variability of APD indicates that factors other than restitution and memory are also important in determining APD during VF.

Amplitude spectrum area: Measuring the probability of successful defibrillation as applied to human data

The objective of our study was to examine the effectiveness of an electrocardiographic predictor, amplitude spectral area (AMSA), for the optimal timing of defibrillation shocks in human victims of cardiac arrest. Based on the spectral characteristics of ventricular fibrillation potentials, we examined the probability of successful conversion to an organized viable rhythm, including the return of spontaneous circulation. The incentive was to predict the likelihood of successful defibrillation and thereby improve outcomes by minimizing interruptions in chest compression and minimizing electrically induced myocardial injury due to repetitive high-current shocks. Observational study on human electrocardiographic recordings during cardiopulmonary resuscitation. Medical research laboratory of a university-affiliated research and educational institute. Victims of out-of-hospital cardiac arrest. Iteration of electrocardiographic records, representing lead 2 equivalent recordings on 108 defibrillation attempts with an automated external defibrillator, of 46 victims of cardiac arrest due to ventricular fibrillation. Three seconds of ventricular fibrillation, recorded immediately preceding delivery of a shock, were analyzed utilizing the AMSA algorithm. AMSA represents a numerical value based on the sum of the magnitude of the weighted frequency spectrum between 3 and 48 Hz. The greater the AMSA value, the greater was the probability of reversal of ventricular fibrillation. At an AMSA value of >13.0 mV-Hz, successful defibrillation yielded a sensitivity of .91 and a specificity of .94. AMSA predicts the success of electrical defibrillation with high specificity. AMSA therefore serves to minimize interruptions of precordial compression and the myocardial damage caused by delivery of repetitive and ineffective electrical shocks.

Cariporide is cardioprotective after iatrogenic ventricular fibrillation in the intact swine heart

Background We sought to introduce sodium–hydrogen exchange inhibition as prophylaxis against the development of ventricular dysfunction in the setting of implantable cardioverter defibrillator insertion in high-risk patients. Cariporide, shown to be safe in humans, was used to reproduce previous results in our laboratory that demonstrated that sodium–hydrogen exchange inhibition preserves left ventricular (LV) function after ventricular fibrillation (VF) and reperfusion. Methods Twelve pigs (weight, 35 to 55 kg) were divided into two groups of six. Baseline ventricular function studies were based on echocardiography, conductance, aortic flow, and LV pressure. Animals were given vehicle (control) or cariporide (3 mg/kg intravenously). Ten minutes later, hearts underwent 80 seconds of VF. After reperfusion for 40 minutes, function studies were repeated. Results Postmortem examination included measuring passive pressure-volume curves and myocardial water content. Systolic indices, including preload recruitable stroke work and ejection fraction, were significantly depressed from baseline after VF and reperfusion for control animals (preload recruitable stroke work, 30.13 ± 0.59 [standard error of the mean] versus 43.85 ± 2.60 mm Hg; ejection fraction, 25.7% ± 2.4% versus 33.5% ± 3.0%) but not for those in the cariporide group (preload recruitable stroke work, 38.36 ± 1.87 versus 40.86 ± 1.45 mm Hg; ejection fraction, 33.9% ± 3.5% versus 32.8% ± 3.9%). In vivo diastolic indices demonstrated trends toward diminished ventricular compliance in control animals but not in the cariporide group after VF and reperfusion. Control animals had significantly increased postmortem LV stiffness, myocardial water content, and normalized LV mass. Conclusions Cariporide preserves LV function after 80 seconds of VF and 40 minutes of reperfusion. Cariporide may prove useful in patients with severe LV dysfunction undergoing VF for implantable cardioverter defibrillator testing.

Sodium-hydrogen exchange inhibition preserves ventricular function after ventricular fibrillation in the intact swine heart

Background: We tested the hypothesis that sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after ischemia-reperfusion injury in the intact porcine heart. Methods: Twelve pigs (weight, 30-45 kg) were evenly divided into 2 groups. Baseline ventricular function studies were based on echocardiography, conductance, aortic flow, and left ventricular pressure. Animals were given vehicle (control) or benzamide-N-(aminoiminomethl)-4-(4-[2-furanylcarbonyl]-1-piperazinyl)-3-(methylsulfonyl)methanesulfonate (BIIB 513; 3 mg/kg administered intravenously). Ten minutes later, hearts were subjected to 75 seconds of ventricular fibrillation. After reperfusion for 40 minutes, function studies were repeated. Hearts were arrested and excised. Postmortem data included passive pressure-volume curves and myocardial water content. Results: Preload recruitable stroke work was significantly decreased from baseline after ischemia and reperfusion in the control group (27.7 ± 2.5 vs 48.0 ± 5.6 mm Hg [± SEM], P = .001) but not in the BIIB 513 group (43.0 ± 5.8 vs 45.5 ± 4.1 mm Hg, P = not significant). In vivo diastolic and postmortem passive left ventricular compliance were reduced after ischemia and reperfusion for control animals but remained unchanged for animals receiving BIIB 513. Time required to recover baseline blood pressure after ventricular fibrillation was significantly longer for control animals (159 ± 15 vs 88 ± 14 seconds [± SEM], P = .008). Myocardial water content (78.97% ± 0.94% vs 77.86% ± 0.46% [± SEM]) and normalized left ventricular mass (137.24 ± 6.17 vs 128.41 ± 1.96 g [± SEM]) were insignificantly increased in control animals. Conclusions: Sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after 75 seconds of ventricular fibrillation and 40 minutes of reperfusion. This family of agents might prove useful in patients with severe left ventricular dysfunction undergoing ventricular fibrillation for implantable cardioverter defibrillator testing.