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Defibrillation Shocks (defibrillation + shock)
Selected AbstractsDefibrillation Causes Immediate Cardiac Dilation in HumansJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003Erin Sylvester B.S. Introduction: Prior studies in isolated heart tissue have shown both excitation and deexcitation to be the primary mechanism of defibrillation. This article presents the first evidence in man of deexcitation immediately following defibrillation by tracking the heart's mechanical response. Methods and Results: The geometric changes of the ventricular chambers were measured before and after defibrillation in seven human subjects receiving an implantable cardioverter defibrillator (ICD). The ICD was used to produce approximately three episodes of ventricular fibrillation and defibrillation in each subject. Twenty-two two-dimensional echocardiographic images of the right ventricle (RV) and 11 images of the left ventricle (LV) were recorded and analyzed at 30 frames per second. Just over 2 seconds of each episode were digitized, beginning half a second before the defibrillation shock. Individual frames were analyzed to yield cross-sectional, ventricular chamber area as a function of time. Immediately following defibrillation, ventricular chambers dilated with significant fractional area increase (RV: 1.58 ± 0.25, LV: 1.10 ± 0.06), with peak dilation at 194 ± 114 msec. Conclusion: Defibrillation causes a rapid increase in ventricular chamber area due to relaxation of the myocardium, suggesting that defibrillation synchronizes the cardiac cells to the deexcited state in man. (J Cardiovasc Electrophysiol, Vol. 14, pp. 832-836, August 2003) [source] Washing Machine Associated 50 Hz Detected As Ventricular Fibrillation by An Implanted Cardioverter DefibrillatorPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2001XAVIER SABATÉ SABATÉ, X., et al.: Washing Machine Associated 50 Hz Detected As Ventricular Fibrillation by An Implanted Cardioverter Defibrillator. This case report describes a patient with an automatic ICD who suffered a defibrillation shock without warning symptoms. An electrical interference can be observed in the stored EGM of the episode. The patient explained that the moment he felt the shock he was touching a washing machine. After correct grounding of this machine the patient did not suffer more inappropriate shocks. [source] Improvement of Defibrillation Efficacy with Preshock Synchronized PacingJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2004HUI-NAM PAK M.D., Ph.D. Introduction: We previously demonstrated that wavefront synchronization by spatiotemporal excitable gap pacing (Sync P) is effective at facilitating spontaneous termination of ventricular fibrillation (VF). Therefore, we hypothesized that a spatiotemporally controlled defibrillation (STCD) strategy using defibrillation shocks preceded by Sync P can improve defibrillation efficacy. Method and Results: We explored the STCD effects in 13 isolated rabbit hearts. During VF, a low-voltage gradient (LVG) area was synchronized by Sync P for 0.92 second. For Sync P, optical action potentials (OAPs) adjacent to four pacing electrodes (10 mm apart) were monitored. When one of the electrodes was in the excitable gap, a 5-mA current was administered from all electrodes. A shock was delivered 23 ms after the excitable gap when the LVG area was unexcitable. The effects of STCD was compared to random shocks (C) by evaluating the defibrillation threshold 50% (DFT50; n = 35 for each) and preshock coupling intervals (n = 208 for STCD, n = 172 for C). Results were as follows. (1) Sync P caused wavefront synchronization as indicated by a decreased number of phase singularity points (P < 0.0001) and reduced spatial dispersion of VF cycle length (P < 0.01). (2) STCD decreased DFT50 by 10.3% (P < 0.05). (3) The successful shocks showed shorter preshock coupling intervals (CI; P < 0.05) and a higher proportion of unexcitable shock at the LVG area (P < 0.001) than failed shocks. STCD showed shorter CIs (P < 0.05) and a higher unexcitable shock rate at LVG area (P < 0.05) than C. Conclusion: STCD improves defibrillation efficacy by synchronizing VF activations and increasing probability of shock delivery to the unexcitable LVG area. (J Cardiovasc Electrophysiol, Vol. 15, pp. 581-587, May 2004) [source] Reentry Site During Fibrillation Induction in Relation to Defibrillation Efficacy for Different Shock WaveformsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2001Ph.D., RAYMOND E. IDEKER M.D. Reentry Site and Defibrillation Waveform Efficacy.Introduction: Unsuccessful defibrillation shocks may reinitiate fibrillation by causing postshock reentry. Methods and Results: To better understand why some waveforms are more efficacious for defibrillation, reentry was induced in six dogs with 1-, 2-, 4-, 8-, and 16-msec monophasic and 1/1- (both phases 1 msec) 2/2-, 4/4-, and 8/8-msec biphasic shocks. Reentry was initiated by 141 ± 15 V shocks delivered from a defibrillator with a 150- , F capacitance during the vulnerable period of paced rhythm (183 ± 12 msec after the last pacing stimulus). The shock potential gradient field was orthogonal to the dispersion of refractoriness. Activation was mapped with 121 electrodes covering 4 × 4 cm of the right ventricular epicardium, and potential gradient and degree of recovery of excitability were estimated at the sites of reentry. Defibrillation thresholds (DFTs) were estimated by an up-down protocol for the same nine waveforms in eight dogs internally and in nine other dogs externally. DFT voltages for the different waveforms were positively correlated with the magnitude of shock potential gradient and negatively correlated with the recovery interval at the site at which reentry was induced by the waveform during paced rhythm for both internal (DFT = 1719 + 64.5 , V , 11.1RI; R2= 0.93) and external defibrillation (DFT = 3445 + 150 , V , 22RI; R2= 0.93). Conclusion: The defibrillation waveforms with the lowest DFTs were those that induced reentry at sites of low shock potential gradient, indicating efficacious stimulation of myocardium. Additionally, the site of reentry induced by waveforms with the lowest DFTs was in myocardium that was more highly recovered just before the shock, perhaps because this high degree of recovery seldom occurs during defibrillation due to the rapid activation rate during fibrillation. [source] Electrophysiologic Deterioration After One-Minute Fibrillation Increases Relative Biphasic Defibrillation EfficacyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000OSCAR H. TOVAR M.D. Biphasic Shocks and One-Minute Fibrillation. Introduction: The probability of survival decreases to 70% after 2 minutes of ventricular fibriltation. Bipliasic shocks are more effective than monophasic shocks in terminating short-duration (<30 sec) ventricular fibrillation. We tested the hypotheses that developing ischemia changes the electrophysiologic characteristics of fibrillation and that the relative efficacy of biphasic shocks increases as electrophysiologic characteristics deteriorate. Methods and Results: Monophasic (12 msec) and biphasic (6/6 msec) shocks (1 to 4 A) were tested in random order in isolated rabbit hearts after 1-minute ischemic fibrillation. Monophasic action potentials showed only a sporadic occurrence of electrical diastole after 5 seconds of fibrillation (24% of action potentials in the right ventricle and 18% in the left ventricle). After 60 seconds of fibrillation, diastole (17.83 ± 1.14 msec in the right ventricle and 21.52 ± 1.16 msec in the left ventricle) appeared after almost every action potential (P < 0.0001 compared with 5 sec), despite a lack of change in fibrillation cycle length and dominant frequency. Monophasie I50 was 2.89 A, and biphasic I50 was 1.4 A (77% reduction in energy). Normalized curve width decreased 28%. Retrospective analysis showed that shocks delivered early in the fibrillation action potential bad a greater probability of succeeding (89%) than shocks delivered late (30%; P < 0.001). Conclusion: After l-minute ischemic fibrillation, diastolic intervals occur during fibrillation. Therefore, defibrillation shocks have an approximately 29% probability of interacting with the fibrillation action potential during diastole. At this time, biphasic shocks produced a more deterministic defibrillation threshold and became even more efficacious (I50B/M = 0.48) than at short fibrillation durations (I50 B/M = 0.7). [source] Procainamide and Survival in Ventricular Fibrillation Out-of-hospital Cardiac ArrestACADEMIC EMERGENCY MEDICINE, Issue 6 2010David T. Markel Abstract Objectives:, Procainamide is an antiarrhythmic drug of unproven efficacy in cardiac arrest. The association between procainamide and survival from out-of-hospital cardiac arrest was investigated to better determine the drug's potential role in resuscitation. Methods:, The authors conducted a 10-year study of all witnessed, out-of-hospital, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) cardiac arrests treated by emergency medical services (EMS) in King County, Washington. Patients were considered eligible for procainamide if they received more than three defibrillation shocks and intravenous (IV) bolus lidocaine. Four logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CI) describing the relationship between procainamide and survival. Results:, Of the 665 eligible patients, 176 received procainamide, and 489 did not. On average, procainamide recipients received more shocks and pharmacologic interventions and had lengthier resuscitations. Adjusted for their clinical and resuscitation characteristics, procainamide recipients had a lower likelihood of survival to hospital discharge (OR = 0.52; 95% CI = 0.36 to 0.75). Further adjustment for receipt of other cardiac medications during resuscitation negated this apparent adverse association (OR = 1.02; 95% CI = 0.66 to 1.57). Conclusions:, In this observational study of out-of-hospital VF and pulseless VT arrest, procainamide as second-line antiarrhythmic treatment was not associated with survival in models attempting to best account for confounding. The results suggest that procainamide, as administered in this investigation, does not have a large impact on outcome, but cannot eliminate the possibility of a smaller, clinically relevant effect on survival. ACADEMIC EMERGENCY MEDICINE 2010; 17:617,623 © 2010 by the Society for Academic Emergency Medicine [source] | ||||||||||