Electroporation induced by internal defibrillation shock with and without recovery in intact rabbit hearts

Defibrillation shocks from implantable cardioverter defibrillators can be lifesaving but can also damage cardiac tissues via electroporation. This study characterizes the spatial distribution and extent of defibrillation shock-induced electroporation with and without a 45-min postshock period for cell membranes to recover. Langendorff-perfused rabbit hearts (n = 31) with and without a chronic left ventricular (LV) myocardial infarction (MI) were studied. Mean defibrillation threshold (DFT) was determined to be 161.4 ± 17.1 V and 1.65 ± 0.44 J in MI hearts for internally delivered 8-ms monophasic truncated exponential (MTE) shocks during sustained ventricular fibrillation (>20 s, SVF). A single 300-V MTE shock (twice determined DFT voltage) was used to terminate SVF. Shock-induced electroporation was assessed by propidium iodide (PI) uptake. Ventricular PI staining was quantified by fluorescent imaging. Histological analysis was performed using Masson's Trichrome staining. Results showed PI staining concentrated near the shock electrode in all hearts. Without recovery, PI staining was similar between normal and MI groups around the shock electrode and over the whole ventricles. However, MI hearts had greater total PI uptake in anterior (P < 0.01) and posterior (P < 0.01) LV epicardial regions. Postrecovery, PI staining was reduced substantially, but residual staining remained significant with similar spacial distributions. PI staining under SVF was similar to previously studied paced hearts. In conclusion, electroporation was spatially correlated with the active region of the shock electrode. Additional electroporation occurred in the LV epicardium of MI hearts, in the infarct border zone. Recovery of membrane integrity postelectroporation is likely a prolonged process. Short periods of SVF did not affect electroporation injury.     

The role of photon scattering in optical signal distortion during arrhythmia and defibrillation

Optical mapping of arrhythmias and defibrillation provides important insights; however, a limitation of the technique is signal distortion due to photon scattering. The goal of this experimental/simulation study is to investigate the role of three-dimensional photon scattering in optical signal distortion during ventricular tachycardia (VT) and defibrillation. A three-dimensional realistic bidomain rabbit ventricular model was combined with a model of photon transport. Shocks were applied via external electrodes to induce sustained VT, and transmembrane potentials (V(m)) were compared with synthesized optical signals (V(opt)). Fluorescent recordings were conducted in isolated rabbit hearts to validate simulation results. Results demonstrate that shock-induced membrane polarization magnitude is smaller in V(opt) and in experimental signals as compared to V(m). This is due to transduction of potentials from weakly polarized midmyocardium to the epicardium. During shock-induced reentry and in sustained VT, photon scattering, combined with complex wavefront dynamics, results in optical action potentials near a filament exhibiting i), elevated resting potential, ii), reduced amplitude relative to pacing, and iii), dual-humped morphologies. A shift of up to 4 mm in the phase singularity location was observed in V(opt) maps when compared to V(m). This combined experimental/simulation study provides an interpretation of optical recordings during VT and defibrillation.     

Mechanisms of superiority of ascending ramp waveforms: new insights into mechanisms of shock-induced vulnerability and defibrillation

Monophasic ascending ramp (AR) and descending ramp (DR) waveforms are known to have significantly different defibrillation thresholds. We hypothesized that this difference arises due to differences in mechanisms of arrhythmia induction for the two waveforms. Rabbit hearts (n = 10) were Langendorff perfused, and AR and DR waveforms (7, 20, and 40 ms) were randomly delivered from two line electrodes placed 10 mm apart on the anterior ventricular epicardium. We optically mapped cellular responses to shocks of various strengths (5, 10, and 20 V/cm) and coupling intervals (CIs; 120, 180, and 300 ms). Optical mapping revealed that maximum virtual electrode polarization (VEP) was reached at significantly different times for AR and DR of the same duration (P < 0.05) for all tested CIs. As a result, VEP for AR were stronger than for DR at the end of the shock. Postshock break excitation resulting from AR generated faster propagation and typically could not form reentry. In contrast, partially dissipated VEP resulting from DR generated slower propagation; the wavefront was able to propagate into deexcited tissue and thus formed a shock-induced reentry circuit. Therefore, for the same delivered energy, AR was less proarrhythmic compared with DR. An active bidomain model was used to confirm the electrophysiological results. The VEP hypothesis explains differences in vulnerability associated with monophasic AR and DR waveforms and, by extension, the superior defibrillation efficacy of the AR waveform compared with the DR waveform.     

Improved ECG detection of presence and severity of right ventricular pressure load validated with cardiac magnetic resonance imaging

The study aimed to assess whether the 12-lead ECG-derived ventricular gradient, a vectorial representation of ventricular action potential duration heterogeneity directed toward the area of shortest action potential duration, can improve ECG diagnosis of chronic right ventricular (RV) pressure load. ECGs from 72 pulmonary arterial hypertension patients recorded <30 days before onset of therapy were compared with ECGs from matched healthy control subjects (n = 144). Conventional ECG criteria for increased RV pressure load were compared with the ventricular gradient. In 38 patients a cardiac magnetic resonance (CMR) study had been performed within 24 h of the ECG. By multivariable analysis, combined use of conventional ECG parameters (rsr' or rsR' in V1, R/S > 1 with R > 0.5 mV in V1, and QRS axis >90 degrees ) had a sensitivity of 89% and a specificity of 93% for presence of chronic RV pressure load. However, the ventricular gradient not only had a higher diagnostic accuracy for chronic RV pressure load by receiver operating characteristic analysis [areas under the curve (AUC) = 0.993, SE 0.004 vs. AUC = 0.945, SE 0.021, P < 0.05], but also discriminated between mild-to-moderate and severe RV pressure load. CMR identified an inverse relation between the ventricular gradient and RV mass, and a trend toward a similar relation with RV volume. In conclusion, chronically increased RV pressure load is electrocardiographically reflected by an altered ventricular gradient associated with RV remodeling-related changes in ventricular action potential duration heterogeneity. The use of the ventricular gradient allows ECG detection of even mildly increased RV pressure load.     

The effect of lidocaine and bretylium on the defibrillation threshold during cardiac arrest and cardiopulmonary resuscitation

The effect of intravenous lidocaine, 2 mg/kg, and bretylium, 5 mg/kg, on defibrillation threshold (DFT) was investigated in alpha-chloralose anesthetized dogs undergoing conventional closed chest cardiopulmonary resuscitation (CPR) following induced ventricular fibrillation. Ventricular fibrillation was induced electrically and CPR was performed by a pneumatic device set to compress the chest 60 times and inflate the lung 12 times a minute. Defibrillation was achieved using underdamped sinusoidal current shocks from a special defibrillator which allowed determination of delivered energy. The DFT was defined as the peak current which defibrillated, but no more than 20% higher than a current which did not defibrillate. All DFTs were obtained within 5 min of CPR. The mean +/- SD current and energy thresholds required for defibrillation during lidocaine-CPR (seven dogs) were 17.0 +/- 8.9 A and 53.0 +/- 40.7 J as compared to 12.5 +/- 6.2 A and 34.3 +/- 30.7 J, respectively during control-CPR (P less than 0.05). The mean +/- SD current and energy thresholds during bretylium-CPR were 11.0 +/- 3.4 A and 24.1 +/- 1.3 J as compared to 11.8 +/- 1.7 A and 29.4 +/- 9.6 J, respectively, during control-CPR (NS). These results show that lidocaine acutely elevated defibrillation threshold whereas bretylium did not produce such an effect. The effect on DFT along with other pharmacologic properties should be considered when lidocaine or bretylium is used in the setting of cardiac arrest and CPR.     

Mechanisms of unpinning and termination of ventricular tachycardia

High-energy defibrillation shock is the only therapy for ventricular tachyarrhythmias. However, because of adverse side effects, lowering defibrillation energy is desirable. We investigated mechanisms of unpinning, destabilization, and termination of ventricular tachycardia (VT) by low-energy shocks in isolated rabbit right ventricular preparations (n = 22). Stable VT was initiated with burst pacing and was optically mapped. Monophasic "unpinning" shocks (10 ms) of different strengths were applied at various phases throughout the reentry cycle. In 8 of 22 preparations, antitachycardia pacing (ATP: 8-20 pulses, 50-105% of period, 0.8-10 mA) was also applied. Termination of reentry by ATP was achieved in only 5 of 8 preparations. Termination by unpinning occurred in all 22 preparations. Rayleigh's test showed a statistically significant unpinning phase window, during which reentry could be unpinned and subsequently terminated with E80 (magnitude at which 80% of reentries were unpinned) = 1.2 V/cm. All reentries were unpinned with field strengths < or = 2.4 V/cm. Unpinning was achieved by inducing virtual electrode polarization and secondary sources of excitation at the core of reentry. Optical mapping revealed the mechanisms of phase-dependent unpinning of reentry. These results suggest that a 20-fold reduction in energy could be achieved compared with conventional high-energy defibrillation and that the unpinning method may be more effective than ATP for terminating stable, pinned reentry in this experimental model.     

Open-thorax guinea pig model for defibrillation

BACKGROUND AND PURPOSE: Guinea pigs are used as models for study of ventricular tachyarrhythmias (VT); however, the tachyarrhythmia often is transient and does not persist. We developed an open-thorax guinea pig model of sustained ventricular fibrillation (VF). METHODS: Bilateral thoracotomy was performed on eight guinea pigs weighing 865 to 1,464 g, and two sutures were positioned in the right ventricular apex for the purpose of pacing. Two methods were used to induce VF: a 50-Hz burst (normal pacing), and an initial 15 beats at 70% of the R-R interval followed by a 100-Hz burst for 84 beats (rapid pacing). Fifteen attempts at inducing VF were performed by use of each method. Blood pressure was recorded before and after development of VF, which was defined as VT with mean blood pressure consistently <10 mm Hg. A final observation was obtained using the normal pacing method without defibrillation. RESULTS: Use of both methods successfully induced VF. A significant relationship between body weight >1,021 g and ability to sustain and survive VF was detected. CONCLUSION: The guinea pig is a useful rodent model for the study of VF and defibrillation.     

Evolution of the optimum bidirectional (+/- biphasic) wave for defibrillation

Introduction of the asymmetric bidirectional (+/- biphasic) current waveform has made it possible to achieve ventricular defibrillation with less energy and current than are needed with a unidirectional (monophasic) waveform. The symmetrical bidirectional (sinusoidal) waveform was used for the first human-heart defibrillation. Subsequent studies employed the underdamped and overdamped sine waves, then the trapezoidal (monophasic) wave. Studies were then undertaken to investigate the benefit of adding a second identical and inverted wave; little success rewarded these efforts until it was discovered that the second inverted wave needed to be much less in amplitude to lower the threshold for defibrillation. However, there is no physiologic theory that explains the mechanism of action of the bidirectional wave, nor does any theory predict the optimum amplitude and time dimensions for the second inverted wave. The authors analyze the research that shows that the threshold defibrillation energy is lowest when the charge in the second, inverted phase is slightly more than a third of that in the first phase. An ion-flux, spatial-K+ summation hypothesis is presented that shows the effect on myocardial cells of adding the second inverted current pulse.     

Left ventricular geometry immediately following defibrillation: shock-induced relaxation

A previous two-dimensional (2D) ultrasound study suggested that there is relaxation of the myocardium after defibrillation. The 2D study could not measure activity occurring within the first 33 ms after the shock, a period that may be critical for discriminating between shock- and excitation-induced relaxation. The objective of our study was to determine the left ventricular (LV) geometry during the first 33 ms after defibrillation. Biphasic defibrillation shocks were delivered 5-50 s after the induction of ventricular fibrillation in each of the seven dogs. One-dimensional, short-axis ultrasound images of the LV cavity were acquired at a rate of 250 samples/s. The LV cavity diameter was computed from 32 ms before to 32 ms after the shock. Preshock and postshock percent changes in LV diameter were analyzed as a function of time with the use of regression analysis. The normalized mean pre- and postshock slopes (0.2 +/- 2.2 and 3.3 +/- 7.9% per 10 ms) were significantly different (P < 0.01). The postshock slope was positive (P < 0.005). Our results confirm that the bulk of the myocardium is relaxing immediately after defibrillation.     

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation

The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1-10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After beta-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without beta-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after beta-blockade. We conclude that a burst of 15-30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. beta-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.     

A 2D FE model of the heart demonstrates the role of the pericardium in ventricular deformation

During pulmonary artery constriction (PAC), an experimental model of acute right ventricular (RV) pressure overload, the interventricular septum flattens and inverts. Finite element (FE) analysis has shown that the septum is subject to axial compression and bending when so deformed. This study examines the effects of acute PAC on the left ventricular (LV) free wall and the role the pericardium may play in these effects. In eight open-chest anesthetized dogs, LV, RV, aortic, and pericardial pressures were recorded under control conditions and with PAC. Model dimensions were derived from two-dimensional echocardiography minor-axis images of the heart. At control (pericardium closed), FE analysis showed that the septum was concave to the LV; stresses in the LV, RV, and septum were low; and the pericardium was subject to circumferential tension. With PAC, RV end-diastolic pressure exceeded LV pressure and the septum inverted. Compressive stresses developed circumferentially in the septum out to the RV insertion points, forming an arch-like pattern. Sharp bending occurred near the insertion points, accompanied by flattening of the LV free wall. With the pericardium open, the deformations and stresses were different. The RV became much larger, especially with PAC. With PAC, the arch-like circumferential stresses still developed in the septum, but their magnitudes were reduced, compared with the pericardium-closed case. There was no free wall inversion and flattening was less. From these FE results, the pericardium has a significant influence on the structural behavior of the septum and the LV and RV free walls. Furthermore, the deformation of the heart is dependent on whether the pericardium is open or closed.     

Virtual electrode polarization in the far field: implications for external defibrillation

We recently suggested that failure of implantable defibrillation therapy may be explained by the virtual electrode-induced phase singularity mechanism. The goal of this study was to identify possible mechanisms of vulnerability and defibrillation by externally applied shocks in vitro. We used bidomain simulations of realistic rabbit heart fibrous geometry to predict the passive polarization throughout the heart induced by external shocks. We also used optical mapping to assess anterior epicardium electrical activity during shocks in Langendorff-perfused rabbit hearts (n = 7). Monophasic shocks of either polarity (10-260 V, 8 ms, 150 microF) were applied during the T wave from a pair of mesh electrodes. Postshock epicardial virtual electrode polarization was observed after all 162 applied shocks, with positive polarization facing the cathode and negative polarization facing the anode, as predicted by the bidomain simulations. During arrhythmogenesis, a new wave front was induced at the boundary between the two regions near the apex but not at the base. It spread across the negatively polarized area toward the base of the heart and reentered on the other side while simultaneously spreading into the depth of the wall. Thus a scroll wave with a ribbon-shaped filament was formed during external shock-induced arrhythmia. Fluorescent imaging and passive bidomain simulations demonstrated that virtual electrode polarization-induced scroll waves underlie mechanisms of shock-induced vulnerability and failure of external defibrillation.     

Success and failure of biphasic shocks: results of bidomain simulations.

The mechanisms behind the superiority of optimal biphasic defibrillation shocks over monophasic are not fully understood. This simulation study examines how the shock polarity and second-phase magnitude of biphasic shocks influence the virtual electrode polarization (VEP) pattern, and thus the outcome of the shock in a bidomain model representation of ventricular myocardium. A single spiral wave is initiated in a two-dimensional sheet of myocardium that measures 2 x 2 cm(2). The model incorporates non-uniform fiber curvature, membrane kinetics suitable for high strength shocks, and electroporation. Line electrodes deliver a spatially uniform extracellular field. The shocks are biphasic, each phase lasting 10 ms. Two different polarities of biphasic shocks are examined as the first-phase configuration is held constant and the second-phase magnitude is varied between 1 and 10 V/cm. The results show that for each polarity, varying the second-phase magnitude reverses the VEP induced by the first phase in an asymmetric fashion. Further, the size of the post-shock excitable gap is dependent upon the second-phase magnitude and is a factor in determining the success or failure of the shock. The maximum size of a post-shock excitable gap that results in defibrillation success depends on the polarity of the shock, indicating that the refractoriness of the tissue surrounding the gap also contributes to the outcome of the shock.     

Mechanistic inquiry into decrease in probability of defibrillation success with increase in complexity of preshock reentrant activity

Energy requirements for successful antiarrhythmia shocks are arrhythmia specific. However, it remains unclear why the probability of shock success decreases with increasing arrhythmia complexity. The goal of this research was to determine whether a diminished probability of shock success results from an increased number of functional reentrant circuits in the myocardium, and if so, to identify the responsible mechanisms. To achieve this goal, we assessed shock efficacy in a bidomain defibrillation model of a 4-mm-thick slice of canine ventricles. Shocks were applied between a right ventricular cathode and a distant anode to terminate either a single scroll wave (SSW) or multiple scroll waves (MSWs). From the 160 simulations conducted, dose-response curves were constructed for shocks given to SSWs and MSWs. The shock strength that yielded a 50% probability of success (ED(50)) for SSWs was found to be 13% less than that for MSWs, which indicates that a larger number of functional reentries results in an increased defibrillation threshold. The results also demonstrate that an isoelectric window exists after both failed and successful shocks; however, shocks of strength near the ED(50) value that were given to SSWs resulted in 16.3% longer isoelectric window durations than the same shocks delivered to MSWs. Mechanistic inquiry into these findings reveals that the two main factors underlying the observed relationships are 1) smaller virtual electrode polarizations in the tissue depth, and 2) differences in preshock tissue state. As a result of these factors, intramural excitable pathways leading to delayed breakthrough on the surface were formed earlier after shocks given to MSWs compared with SSWs and thus resulted in a lower defibrillation threshold for shocks given to SSWs.     

Developmental changes of ventricular fibrillation threshold and spontaneous defibrillation in young dogs.

This study was conducted to systematically investigate whether induction and maintenance of ventricular fibrillation in the canine heart, change with age during the early postnatal development. Forty-eight mongrel puppies from seven litters, were randomly selected for size and studied at weekly intervals from 1-6 weeks for determination of ventricular fibrillation threshold and incidence of spontaneous defibrillation. Another fourteen mongrel puppies 8-11 weeks old and 10 adult dogs were similarly studied. Ventricular fibrillation threshold increased progressively with age up to the eighth week (VFTmA = 8.38 + 2.67 wk-0.134.wk2, r = 0.995) and thereafter reached a plateau, which was not significantly different from the ventricular fibrillation threshold of adult dogs (26.5 +/- 2.2 mA). In contrast, the high incidence of spontaneous defibrillation at early age decreased rapidly between second and fourth week and became rare thereafter, (%SDF = 281.e-0.60wk, r = 0.94. This rapid drop could not be explained by the increase in mean body weight, which did not change significantly during this early period (BWkg = 0.59.e0.23wk, r = 0.97). Our findings suggest first, that the vulnerability of the neonatal dog heart to electrical induction of ventricular fibrillation decreases progressively during early age. Second, that spontaneous defibrillation decreases precipitously between the second and fourth week of age, a change not sufficiently explained by the modest body weight gain during that time. Thus, it appears that about the third week of age ventricular vulnerability to fibrillation and ability to defibrillation reach a critical point, where lethal arrhythmias may become both inducible and sustainable, to result in death.     

Transthoracic ventricular defibrillation in adults.

A prospective study of the energy required for transthoracic ventricular defibrillation in adults showed that in 42 (81%) out of 52 episodes of ventricular fibrillation shocks of 100 watt-seconds (Ws) of stored energy were successful. Out of 233 episodes, 222 (95%) were converted by 200 W s shocks. Among patients in whom primary ventricular fibrillation occurred within one hour of the onset of acute myocardial infarction, 200 W s shocks were successful in 40 (98%) out of 41 episodes. When low-energy shocks failed, a stored energy of 400 W s invariably succeeded. The need for large and expensive defibrillators that store more than 400 W s and are less readily available is therefore questioned.     

The effect of spatial scale of resistive inhomogeneity on defibrillation of cardiac tissue

Defibrillation of cardiac tissue can be viewed in the context of dynamical systems theory as the attempt to move a dynamical system from the basin of attraction of one attractor (fibrillation) to another (the uniform rest state) by applying a stimulus whose form is physically constrained. Here we give an introduction to the physical mechanism of cardiac defibrillation from this dynamical perspective and examine the role of resistive inhomogeneity on defibrillation efficacy. Using numerical simulations with rotating waves on a one-dimensional periodic ring, we study the role of the spatial scale of resistive inhomogeneity on defibrillation. For a rotating wave on a periodic ring there are three stable attractors, namely the uniform rest state, a wave traveling clockwise and a wave traveling counterclockwise. As a result, the application of a stimulus has the potential for three different outcomes, namely elimination of the wave, phase resetting of the wave, and reversal of the wave. The results presented here show that with resistive inhomogeneities of large spatial scale, all three of these transitions are possible with large amplitude shocks, so that the probability of defibrillation is bounded well below one, independent of stimulus amplitude. On the other hand, resistive inhomogeneities of small spatial scale produce a defibrillation threshold that is qualitatively consistent with that found experimentally, namely the probability of defibrillation success is an increasing function that approaches one for large enough stimulus amplitude. Extending these results to higher dimensions, we describe conditions for successful defibrillation of functional reentry with large scale spatial inhomogeneity, but find that elimination of anatomical reentry is quite difficult. With small spatial scale inhomogeneity, there are no similar restrictions.     

Current required for ventricular defibrillation.

The mean current required for ventricular defibrillation was measured and found to be 0.35 +/- SE 0.03 A/kg body weight, which is about one-third of that predicted from animal experiments. There was no apparent correlation between the current required and body weight (r = -0.007 +/- SE 0.213). There is no evidence of need for defibrillators storing more than 400 J.     

Optimal parameters for electrical auricular defibrillation

In acute experiments on dogs the chest was opened and auricular flutter and fibrillation were induced. Current, energy and charge thresholds which eliminated this arrhythmia by the monopolar direct impulse of 1--15 ms duration were determined. The current and energy values that evoked the auricular defibrillation during direct application of the electrodes to them were minimal when the impulses of 8 ms were used: 113 +/- 13.7 mA and 10.4 +/- 2.6 mWs in elimination of the flutter, and 275 +/- 18.2 mA and 62.3 +/- +/- 9.0 mWsec in elimination of the fibrillation. The current that restored the nomotopic rhythm during direct auricular defibrillation was 50 times less than that determined during the transthoracic auricular defibrillation in dogs. The efficacy of direct auricular defibrillation indicated the necessity of the elaboration of an adequate method for its application in clinical practice.     

Numerical Simulation of Dynamic Electro-Mechanical Response of Ionic Polymer-Metal Composites

Ionic Polymer-Metal Composites (IPMC) is an emerging class of Electro-Active Polymer (EAP) materials. IPMC has attractive features, such as high sensitivity and light weight, which are useful for developing novel designs in the fields of bionic actuators, artificial muscles and dynamic sensors. A Finite Element (FE) model was developed for simulating the dynamic electro-mechanical response of an IPMC structure under an external voltage input. A lumped Resistor-Capacitor (RC) model was used to describe the voltage-to-current relationship of a Nafion IPMC film for the computation of electric field intensity. Moreover, the viscoelastic property of the IPMC film was considered in the model and the non-uniform bending behavior was also taken into account. Based on the proposed model and the assumption that the thicknesses of the two electrodes are the same and uniform, the optimal coating thickness of the IPMC electrode was determined. It was demonstrated that the dynamic electro-mechanical response of the IPMC structure can be predicted by the proposed FE model, and the simulation results were in good agreement with the experimental findings.