Gregory P. Walcott

Choosing the optimal monophasic and biphasic waveforms for ventricular defibrillation.

Optimal Monophasic and Biphasic Waveforms. Introduction: The truncated exponential waveform from an implantable cardioverter defibrillator can be described by three quantities: the leading edge voltage, the waveform duration, and the waveform time coastant (τs). The goal of this work was to develop and test a mathematical model of defibrillation that predicts the optimal durations for monophasic and the first phase of biphasic waveforms for different τs values. In 1932, Blair used a parallel resistor‐capacitor network as a model of the cell membrane to develop an equation that describes stimulation using square waves. We extended Blairs model of stimulation, using a resistor‐capacitor network time constant (τm), equal to 2.8 msec, to explicitly account for the waveform shape of a truncated exponential waveform. This extended model predicted that for monophasic waveforms with τs of 1.5 msec, leading edge voltage will be constant for waveforms 2 msec and longer; for τs of 3 msec, leading edge voltage will be constant for waveforms 3 msec and longer; for τs of 6 msec, leading edge voltage will be constant for waveforms 4 msec and longer. We hypothesized that the best phase 1 of a biphasic waveform is the best monophasic waveform. Therefore, the optimal first phase of a biphasic waveform for a given τs is the same as the optimal monophasic waveform.

Comparison of the temperature profile and pathological effect at unipolar, bipolar and phased radiofrequency current configurations

With a multi-electrode catheter, phased radiofrequency (RF) delivers current between each electrode and a backplate as well as between adjacent electrodes. This study compared the tissue heating and lesion dimensions created by phased and standard RF. Ablation was performed on the in vivo thigh muscles in 5 pigs. Six lesions were created on each thigh muscle using phase angle 0° RF, 127° RF, 180° RF with and without a backplate, and standard RF in bipolar and sequential unipolar configurations. Two plunge needles, each with 6 thermocouples 1mm apart, were inserted into the tissue with one needle beside an electrode and the other midway between electrodes for tissue temperature measurement. The 0° RF created lower tissue temperatures and smaller lesions between electrodes than those beside electrode. With 127° and 180° RF, tissue temperature and lesion dimensions between electrodes were similar to beside electrode, while the 127° RF created higher tissue temperature and deeper lesions than 180° RF (both with and without a backplate) at both sites. Standard RF bipolar ablation created similar tissue temperatures and lesion depths at both sites, but required greater power than the 127° RF. Standard RF sequential unipolar ablation created only a slight temperature increase and no lesions between electrodes 3 and 4. As judged by tissue temperature, lesion depth and uniformity, and RF power requirement, 127° RF may be a better energy configuration for linear ablation than the other RF modalities tested.

Electrode Impedance: An Indicator of Electrode-Tissue Contact and Lesion Dimensions During Linear Ablation

Pre-ablation impedance was evaluated for its ability to detect electrode-tissue contact and allow creation of long uniform linear lesions with a multi-electrode ablation catheter. The study consisted of 2 parts, both of which used the in vivopig thigh muscle model. In part 1, a 7 Fr. multi-electrode catheter was held in 3 electrode-tissue contact conditions: (1) non-contact; (2) light contact with a 30[emsp4 ]g downward force; and (3) tight contact with a 90[emsp4 ]g downward force. Impedances were measured in unipolar, modified unipolar and bipolar configurations using a source with frequencies from 100[emsp4 ]Hz to 500[emsp4 ]kHz. Compared with non-contact, the impedance increased 35±22±% with 30[emsp4 ]g contact pressure and 68±40±% when the contact pressure was increased to 90[emsp4 ]g across the range of frequencies studied. In part 2, the same catheter was held against the tissue with different forces. Pre-ablation impedance was measured using a 10[emsp4 ]kHz current. Phased radiofrequency energy was applied to the 5 electrodes simultaneously using 10[emsp4 ]W power at each electrode for 120[emsp4 ]s. A total of 32 linear lesions were created. The lesion dimensions correlated with pre-ablation impedance. A unipolar impedance ≥190[emsp4 ]Ω indicates 95±% possibility to create a uniform linear lesion of at least 3[emsp4 ]mm depth with our ablation system. We conclude that pre-ablation impedance may be a useful indicator for predicting electrode-tissue contact and the ability to create a continuous and transmural linear lesion with a multi-electrode catheter.

Pulseless electric activity: Definition, causes, mechanisms, management, and research priorities for the next decade: Report from a national heart, lung, and blood institute workshop

Sudden cardiac arrest (SCA) remains an important public health challenge. Despite a dramatic decrease in the age-adjusted risk of SCA, the cumulative number of fatal SCAs in the United States remains large. Estimates range from 450 000 fatal SCAs per year; a figure in the range of 300 000 to 370 000 per year is likely the best current estimate.1 SCA appears to account for ≈50% of all cardiovascular deaths,2 and it is estimated that 50% of the SCAs are the first clinical expression of previously undiagnosed heart disease.2,3 Most out-of-hospital cardiac arrests (80%) occur in private homes or other living facilities.4 Electric mechanisms associated with SCA are broadly classified into tachyarrhythmic and nontachyarrhythmic categories, the latter including pulseless electric activity (PEA; formerly referred to as electromechanical dissociation), asystole, extreme bradycardia, and other mechanisms often associated with noncardiac factors (Table). The first approaches to the problem of SCA focused on ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). An early impact on the prevention and treatment of VF and VT was realized in patients with acute coronary syndromes >50 years ago,5 followed by the development of strategies for responding to out-of-hospital cardiac arrest, implantable cardioverter-defibrillators, and defibrillation by lay responders. View this table: Table. Tachyarrhythmic and Nontachyarrhythmic Cardiac Arrest Data from the Seattle emergency rescue system6 and elsewhere7–9 have identified progressive reductions in the number of responses to SCA over 2 to 3 decades. This change was due primarily to a reduction in the number of ventricular tachyarrhythmic events identified by emergency medical services responders. In the Seattle data, the incidences of PEA and asystole had not changed over the 3 decades of observation and therefore have emerged as proportionately more frequent mechanisms than VT/VF. Whether this also reflects the …

Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs

Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution (n = 6) or normal Tyrode solution as a control (n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 x 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 +/- 1.5 vs. 9.2 +/- 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.

Impact of Myocardial Ischemia and Reperfusion on Ventricular Defibrillation Patterns, Energy Requirements, and Detection of Recovery

Background—Shocks that have defibrillated spontaneous ventricular fibrillation (VF) during acute ischemia or reperfusion may seem to have failed if VF recurs before the ECG amplifier recovers after shock. This could explain why the defibrillation threshold (DFT) for spontaneous VF appears markedly higher than for electrically induced VF. Methods and Results—The DFT for electrically induced VF (E-DFT) was determined in 15 pigs before ischemia, followed by left anterior ascending or left circumflex artery occlusion. VF was electrically induced 20 minutes after occlusion, followed 5 minutes later by reperfusion. Whether spontaneous or electrically induced, VF during occlusion or reperfusion was treated with up to 3 shocks at 1.5×E-DFT. If all 3 shocks failed, shock strength was increased. Thirty minutes after reperfusion, the other artery was occluded and the protocol was repeated. Defibrillation was considered successful if postshock sinus/idioventricular rhythm was present for ≥30 seconds. VF recurring within 30 seconds after the shock was considered immediate or delayed if the first postshock activation complex in a rapidly restored ECG recording was VF or sinus/idioventricular rhythm, respectively. Defibrillation efficacy at 1.5×E-DFT was significantly higher for electrically induced ischemic VF (76%) than for spontaneous VF (31%). The incidence of delayed recurrence after electrically induced nonischemic (3%) or ischemic (20%) VF was significantly lower than after spontaneous VF (75%). Mean VF recurrence time after spontaneous VF was 4.6±5.3 seconds. Conclusions—Spontaneous VF can be halted by a shock but then quickly restart before a standard ECG amplifier has recovered from postshock saturation, making it appear that the shock failed.

Defibrillation threshold and cardiac responses using an external biphasic defibrillator with pediatric and adult adhesive patches in pediatric-sized piglets

Before recommendations for using an automatic external defibrillator on pediatric patients can be made, a protocol for the energy of a biphasic waveform energy dosing needs to be determined that will allow ventricular defibrillation of 8 year olds while causing only a minimal amount of cardiac damage to infants. Pediatric- and adult-sized electrode patches were alternately applied to 10 isoflurane-anesthetized piglets weighing 3.8-20.1 kg to approximate the body weights of newborns to children < 8 years old. The defibrillation threshold (DFT) was determined for biphasic truncated exponential waveform shocks. Additional shocks, varying from the DFT to 360 Joules (J), were delivered during sinus rhythm or following 30 s of ventricular fibrillation (VF). The DFT was 2.4+/-0.81 and 2.1+/-0.65 J/kg for pediatric and adult patches, respectively (P = N.S.). The change in left ventricular (LV) dP/dt from baseline as a function of shock strength was significantly different at 1 and 10 s after shocks of increasing energy that were delivered in sinus rhythm, and 1, 10, 20, and 30 s after defibrillation shocks. There was no significant difference in LV dP/dt with increasing shock energy at 60 s with either patch size. The time to return of sinus rhythm, ST-segment deviation, and cardiac output were also not significantly different from baseline 60 s following shocks of up to 360 J delivered during sinus rhythm or VF with either patch. The same amount of energy delivered with a biphasic external defibrillator successfully defibrillated VF whether adult or pediatric patches were used. Cardiac rhythm and hemodynamic variables were unaltered at 60 s after shocks delivered at energies of up to 360 J. These data suggest that there is a substantial safety margin above a DFT strength shock for this biphasic waveform in piglets.

Locally Propagated Activation Immediately After Internal Defibrillation

BACKGROUND Electrical mapping studies indicate an interval of 40 to 100 ms between a defibrillation shock and the earliest activation that propagates globally over the ventricles (globally propagated activation, GPA). This study determined whether activation occurs during this interval but propagates only locally before being blocked (locally propagated activation, LPA). METHODS AND RESULTS In five anesthetized pigs, the heart was exposed and a 504-electrode sock with 4-mm interelectrode spacing was pulled over the ventricles. Ten biphasic shocks of a strength near the defibrillation threshold (DFT) were delivered via intracardiac catheter electrodes, and epicardial activation sequences were mapped before and after attempted defibrillation. Local activation was defined as dV/dt < or =-0.5 V/s. Postshock activation times and wave-front interaction patterns were determined with an animated display of dV/dt at each electrode in a computer representation of the ventricular epicardium. LPAs were observed after 40 of the 50 shocks. A total of 173 LPA regions were observed, each of which involved 2+/-2 (mean+/-SD) electrodes. LPAs were observed after both successful and failed shocks but occurred earlier (P<.0001) after failed (35+/-8 ms) than successful (41+/-16 ms) shocks, although the times at which the GPA appeared were not significantly different. On reaching the LPA region, the GPA front either propagated through it (n=135) or was blocked (n=38). The time from the onset of the LPA until the GPA front propagated to reach the LPA region was shorter (P<.01) when the GPA front was blocked (32+/-12 ms) than when it propagated through the LPA region (63+/-20 ms). CONCLUSIONS LPAs exist after successful and failed shocks near the DFT. Thus, the time from the shock to the GPA is not totally electrically silent.

Short-Acting β-Adrenergic Antagonist Esmolol Given at Reperfusion Improves Survival After Prolonged Ventricular Fibrillation

Background—High catecholamine concentrations are cytotoxic to cardiac myocytes. We hypothesized that myocardial interstitial catecholamine levels are greatly elevated immediately after long-duration ventricular fibrillation (VF), defibrillation, and reperfusion and that the short-acting β-antagonist esmolol administered at reperfusion would protect against this catecholamine surge and improve survival. Methods and Results—In part 1 of this study, catecholamines from myocardial interstitial fluid (ISF) and aortic and coronary sinus plasma were quantified by use of 3H-labeled radioenzymatic assay in 8 open-chest, anesthetized pigs. Eight minutes of electrically induced VF was followed by internal defibrillation and reperfusion. By 4 minutes of VF, ISF norepinephrine increased significantly, from 1.3± 0.3 to 7.4± 2.4 ng/mL. Epinephrine increased significantly, from 0.4± 0.2 to 1.5± 0.7 ng/mL. ISF norepinephrine and epinephrine peaked at 219.2± 92.1 and 63.7± 25.1 ng/mL after defibrillation and reperfusion and decreased significantly to 12.2± 3.5 and 6.7± 3.1 ng/mL 23 minutes after defibrillation. Transcardiac catecholamine changes were similar. In part 2, 8 minutes of VF was followed by external defibrillation in anesthetized, closed-chest pigs. Animals received 1.0 mg/kg esmolol (n= 8) or saline (n= 8) intravenously at the start of cardiopulmonary resuscitation (CPR). Advanced cardiac life support, including CPR and epinephrine, was delivered to both groups. Esmolol before reperfusion improved return of spontaneous circulation and 4-hour survival (7/8 versus 3/8 survivors, χ2P < 0.05). Conclusions—Transcardiac and ISF norepinephrine and epinephrine levels are briefly massively elevated after 8 minutes of VF, defibrillation, and reperfusion. A short-acting β-antagonist administered immediately after defibrillation improves return of spontaneous circulation and 4-hour survival after this prolonged VF.

Why Is Catheter Ablation Less Successful than Surgery for Treating Ventricular Tachycardia that Results from Coronary Artery Disease

Nearly 80% of patients with coronary artery disease who have map‐directed surgery for control of ventricular tachycardias require no drug therapy to prevent recurrences, while fewer than 50% of patients undergoing catheter ablation have similar outcomes. Catheter ablation will fail if arrbythmogenic sites are incompletely ablated by lesions that are too small or too far away from the reentrant pathway or if all arrbythmogenic sites are not identified. The underlying assumptions used to guide site selection are that: (a) ventricular tachycardias arise from reentrant mechanisms; (b) monomorphic ventricular tachycardias with similar QRS morphologies arise from the same pathway; (c) the ventricular tachycardia initiated during the procedure represents the patients spontaneous arrhythmia; (d) the endocardial site that should be ablated can be identified from cardiac activation maps produced during induced ventricular tachycardia or from ancillary techniques; and (e) the patient has only one or two reentrant pathways. Relying on incorrect assumptions may account for the difference in success rates. Patients may have similar appearing ventricular tachycardias that arise from different pathways, and the entire thin layer of viable tissue between the infarct and the endocardium may contain many reentrant pathways. Some ventricular tachycardias may arise from the myocardium away from the endocardium, while others may arise from the epicardium. Small lesions may not be large enough to eliminate all possible reentrant pathways. Catheter ablation may be less successful because the lesions are inadequate, the assumptions guiding the selection of arrhythmogenic tissue are incorrect, or all arrhythmogenic sites are not identified. The primary reason catheter ablation is less successful than surgery in the treatment of ventricular tachycardias is that catheter ablation does not ablate as much tissue as is removed by surgery. The success rate of catheter ablation probably can be improved if the amount of tissue ablated is increased.