Myocardial dysfunction after electrical defibrillation

We hypothesized that electrical shocks that defibrillate hearts successfully also produce myocardial injury, but only in settings in which the myocardium is underperfused. Myocardial function was measured in isolated, conventionally perfused or underperfused rat hearts during sinus rhythm and conventionally perfused or underperfused hearts during ventricular fibrillation (VF) after delivery of a sham, a 0.4 J, or a 0.7 J shock. In underperfused hearts, the dP/dt, negative dP/dt, left ventricular diastolic pressure and left ventricular pressure-volume relationships demonstrated significant impairment in myocardial function. Impairment increased with the higher energy shocks. This contrasted with normally perfused hearts, whether in sinus rhythm or during VF, in which shocks resulted in no significant impairment. Electrical shocks therefore produce myocardial injury but only when myocardial perfusion is reduced.     

The nature of electric defibrillation of the heart

It has been shown experimentally that electrical defibrillation of the heart is the result of synchronization of separate heart elements. Bipolar impulses have been found to be the most effective technique for defibrillation. It had the advantage that the excitatory effect was determined by the sum of the amplitude of both half-waves of the current, and the damaging effect was determined only by the value of the first half-wave. The decisive role of the steepness of the rear-front of the impulse on the effect of cardiac defibrillation is also shown.     

Optimal timing for electrical defibrillation after prolonged untreated ventricular fibrillation

OBJECTIVE: It currently is recommended that electrical shocks be delivered immediately on recognition of ventricular fibrillation. However, decreased effectiveness of this approach has been reported after prolonged intervals of untreated ventricular fibrillation. We investigated the optimal strategy for successful defibrillation after prolonged untreated ventricular fibrillation by using a rat model of ventricular fibrillation and closed-chest resuscitation. DESIGN: Controlled, randomized, laboratory study. SETTING: Research laboratory at a VA hospital. SUBJECTS: Seventy pentobarbital anesthetized Sprague-Dawley rats. INTERVENTIONS: After 10 mins of untreated ventricular fibrillation, four groups of rats were randomized to receive electrical shocks (which we designated as "experimental shocks") immediately before or at 2, 4, or 6 mins of chest compression. Unsuccessfully defibrillated rats received additional shocks (which we designated as "rescue shocks") after 8 mins of chest compression. MEASUREMENTS AND MAIN RESULTS: The number of rats that restored spontaneous circulation after the experimental shocks increased with increasing duration of the predefibrillatory interval of chest compression (0 of 8, 0 of 8, 2 of 8, and 7 of 8, respectively, p <.005). Two additional groups then were randomized to receive repetitive experimental shocks at 2, 4, and 6 mins or a single attempt at 6 mins of chest compression. Although a comparable number of rats restored spontaneous circulation in each group, rats subjected to repetitive defibrillation attempts had more intense postresuscitation ectopic activity and worse survival. Two final groups were used to investigate whether inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) could facilitate return of spontaneous circulation during repetitive defibrillation attempts. Although spontaneous circulation was restored earlier in more rats subjected to NHE-1 inhibition, the differences were statistically insignificant. NHE-1 inhibition, however, replicated previously reported resuscitation and postresuscitation benefits. The optimal predefibrillation interval of chest compression was approximately 6 mins, and this coincided with partial return of the amplitude and frequency characteristics of the ventricular fibrillation waveform to those present immediately after induction of ventricular fibrillation. CONCLUSIONS: Improved outcome after prolonged untreated ventricular fibrillation may result from strategies that provide chest compression before attempting defibrillation and avoid early and repetitive defibrillation attempts. The amplitude and frequency characteristics of the ventricular fibrillation waveform could help identify the optimal timing for attempting electrical defibrillation.     

Transthoracic electrical impedance during external defibrillation: comparison of measured and modelled waveforms

The transthoracic electrical impedance is an important defibrillation parameter, affecting the defibrillating current amplitude and energy, and therefore the defibrillation efficiency. A close relationship between transthoracic impedance and defibrillation success rate was observed. Pre-shock measurements (using low amplitude high frequency current) of the impedance were considered a solution for selection of adequate shock voltages or for current-based defibrillation dosage. A recent approach, called 'impedance-compensating defibrillation' was implemented, where the pulse duration was controlled with respect to the impedance measured during the initial phase of the shock. These considerations raised our interest in reassessment of the transthoracic impedance characteristics and the corresponding measurement methods. The purpose of this work is to study the variations of the transthoracic impedance by a continuous measurement technique during the defibrillation shock and comparing the data with results obtained by modelling. Voltage and current impulse waveforms were acquired during cardioversion of patients with atrial fibrillation or flutter. The same type of defibrillation pulse was taken from dogs after induction of fibrillation. The electrodes were located in the anterior position, for both the patients and animals.     

Mechanisms underlying the training effects associated with neuromuscular electrical stimulation

Although neuromuscular electrical stimulation (NMES) can increase the ability of muscle to exert force, the means by which this is accomplished seem to be different from those associated with voluntary exercise. The aim of the study was to determine whether the recruitment order of motor units elicited by over-the-muscle electrical stimulation is different from that achieved with voluntary activation of muscle. This difference was tested by comparing muscle twitch responses that were elicited by Hoffmann reflexes (H-reflexes) and direct motor responses (M-responses) and by examining the effect of submotor NMES on the twitch force associated with H-reflexes. Because H-reflexes represent the summed activity of many motor units, in a manner that is consistent with volitional activation, variation in the time to peak twitch force indicates changes in the population of motor units that contribute to the response. The results demonstrated that the percutaneous application of submotor NMES to the limbs of human subjects causes a faster-contracting population of motor units to be activated during a test H-reflex. Consequently, it seems that the application of NMES preferentially activates faster-contracting motor units, perhaps those that are normally only active at high exercise intensities under voluntary conditions.     

Transvenous biventricular defibrillation can improve defibrillation threshold

A case report of a patient with a high defibrillation threshold at initial implantation that was improved by the insertion of a shocking coil in the left lateral cardiac vein is discussed.     

Multiple interatrial electrical connection after heart transplantation

A 62-year-old woman who underwent heart transplantation 6 years later presented a regular atrial tachycardia. Electrophysiologic evaluation showed an atrial arrhythmia in the recipient atrium with 2:1 conduction to the donor atrium, with a confusing electroanatomical map. With the suspect of alternant conduction through two different breakthroughs, the map was split in two concordant maps, corresponding to two connections that were successfully ablated. Later on, a third connection was detected and therefore ablated.