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Despite frequent arrhythmia and sudden death in heart failure, attempts to study arrhythmia mechanisms in patients are difficult. The dog heart, paced for several weeks at a fast rate to induce heart failure is prone to arrhythmia. The aim of this study was to determine the activation patterns of spontaneous and electrically induced arrhythmia and the susceptibility of the failing dog heart to arrhythmia and early afterdepolarization (EAD) induced triggered activity elicited by exogenous administration of cesium chloride (CsCl). The hearts of 56 mongrel dogs were paced at 240 beats/min for 3-5 weeks (heart failure group). Twenty-one similarly operated, but not paced dogs served as the control group. At baseline, all dogs were healthy as assessed electrophysiologically and hemodynamically. Spontaneous (bradycardia, tachycardia, and arrhythmic deaths) and electrically induced arrhythmia was frequent in dogs with heart failure. Also, the minimal dose of CsCl that produced ventricular tachycardia was significantly lower in the heart failure than the control dogs (1.02 +/- 0.02 vs 1.21 +/- 0.07 mMol/kg, P < 0.05). Epicardial mapping during spontaneous and electrically induced arrhythmia in the heart failure dogs showed initiation patterns with focal origin, often from multiple sites. This pattern was consistent with the patterns observed with CsCl induced ventricular tachycardia. In in vitro microelectrode studies, CsCl superfusion (2.5-5 mMol/L) induced triggered activity due to EADs within 30 minutes, in seven of the eight Purkinje fibers from four heart failure dogs. EADs were also found in ventricular myocytes of papillary muscle from two heart failure dogs. In contrast, 5 mMol/L CsCl induced EADs in only one of eight Purkinje fibers from the hearts of four control dogs and no papillary myocytes even with continuous superfusion for up to 60 minutes (P < 0.01). These results demonstrate that pacing induced heart failure in the dog has an increased tendency to develop ventricular tachycardia and triggered activity unmasked by CsCl.

Current generation implantable cardioverter defibrillators use monophasic, biphasic, or sequential pulse shocks, most of which truncate after a given time, dumping the remaining charge on the capacitor through an internal resistor. We hypothesized that having an additional current pathway, and delivering the majority of the remaining charge on a single capacitor to the two pathways using additional shock phases, would improve defibrillation efficacy. This hypothesis was tested by comparing DFTs using a simulated single capacitor, single-biphasic shock (two 5-ms pulses separated by 0.2 ms), delivered to coupled pairs of electrodes, to those using a sequential-biphasic shock (four 5-ms pulses separated by 0.2 ms) delivered to separate opposing electrodes, delivered from the same electrodes for both waveforms. In eight open-chest anesthetized pigs, four mesh electrodes (Medtronic TX-7, 6.5 cm2), were sutured on the epicardium of the anterior and posterior surfaces of each ventricle. Shocks were delivered from a 200-microF capacitor bank. Triplicate DFTs were obtained using each waveform in a randomized crossover design. Initial leading edge voltage (mean +/- SEM: 420 +/- 33 V vs 497 +/- 34 V; P < 0.05), initial peak current (4.8 +/- 0.4 A vs 13 +/- 1.1 A; P < 0.001), and delivered energy (16.9 +/- 2.6 J vs 30.4 +/- 5.3 J; P < 0.05) at the DFT were all significantly lower using sequential-biphasic shocks than those using single-biphasic shocks, respectively. We conclude that for direct heart defibrillation, it is worthwhile to combine sequential capability to biphasic shocks and deliver the remaining charge on the capacitor to the two different pathways.

The cellular electrophysiological effects of defibrillation shocks on the myocardium during ventricular fibrillation are not clear. The present study investigated the effects of high voltage shocks on membrane potentials of isolated guinea pig and pig papillary muscles during rapid activations simulating ventricular fibrillation. High voltage shocks induced an action potential with a prolonged duration, followed by a transient refractory state. Subsequent action potentials following this refractory state had shortened durations. The duration of the transient refractory state varied in proportion to shock intensity and stimulation rate, whether the shock was biphasic or monophasic. Shock induced prolonged depolarization was not a consistent finding and mainly observed with slow stimulation rates. In conclusion, high voltage shocks induce bimodal changes of the action potential duration associated with a transient refractory state during rapid activation. The rate dependency of this refractory state suggests that the duration of the shock induced refractory state may be longer in the fibrillating than the normal beating heart, and may contribute to successful defibrillation.

This study investigated the influence of defibrillator shocks delivered directly over a coronary artery, independent of ventricular fibrillation, on cardiac hemodynamics. Thirty-six open chest, halothane anesthetized pigs were randomized to receive six shocks at one of 5,0, 7.5, or 10.0 joules (J). Shocks were delivered between two mesh electrodes (Medtronic TX-7) sutured onto the epicardium, one over the left anterior descending coronary artery and the second directly opposite on the posterobasal ventricular surface. Shock delivery was synchronized to the R wave of the cardiac cycle, to reduce the risk of inducing fibrillation, with a 5-minute stabilization period between successive shocks. Pressure from the left ventricle, the left anterior descending coronary artery, distal to the mesh electrode and the left circumflex (control) artery and contractility in the regions perfused by both arteries were measured. The shocks invariably produced an immediate (2-second postshock), but transient, depression in systolic pressure of the same magnitude for the left anterior descending coronary artery, circumflex artery and the left ventricle that recovered by 5-minute postshock. There was no dose dependent relationship to energy. Also there was no clear difference in myocardial wall motion between the area perfused by the left anterior descending coronary artery and that perfused by the circumflex artery. These results suggest that shocks up to 10 J delivered over an epicardial artery do not cause arterial spasm and do not compromise coronary artery blood flow.

During testing of implantable defibrillators, ability to sense ventricular fibrillation is assessed by observing electrograms and the emitted ECG interpretation channel during induced ventricular fibrillation. We hypothesized that ventricular electrogram amplitude in sinus rhythm could be used to predict the ventricular electrogram amplitude in ventricular fibrillation and serve as a first approximation of the “safety margin” for sensing ventricular fibrillation. We compared the peak-to-peak epicardial ventricular electrogram during sinus rhythm and ventricular fibrillation in 12 patients undergoing defibrillator impJantation. The ventricular electrogram was recorded with an integrated bipolar lead and Altered at 10–50 Hz. Ventricular fibrillation was induced by alternating current and the ventricular electrogram measured from cessation of alternating current to the first countershock. The mean ventricular electrogram amplitude in sinus rhythm was 15.3 ± 5.4 mV (range 7.1–25.5) and in 37 episodes of ventricular fibrillation was 8.3 ± 3.6 mV frange 2.1–16.3). There was a significant relationship between the mean ventricular electrogram amplitude in sinus rhythm and in ventricular fibrillation (R = 0.7, P < 0.001). There was wide variation among individuals in the decrease in the mean ventricular electrogram amplitude during ventricular fibrillation, with the ratio of mean ventricular electrogram in sinus rhythm to mean ventricular electrogram in ventricular fibrillation ranging from 0.29 to 1.05 (mean 0.55 ± 0.20). This suggests that up to a fourfold decrease may be expected in the mean ventricular electrogram amplitude during ventricular fibrillation. These results suggest that there is a relationship between the mean ventricular electrogram in sinus rhythm and in ventricular fibrillation which is useful as an initial approximation in assessing sensing lead function and programming device sensitivity levels.

We assessed the value and safety of using a low voltage test shock to predict cardiac and electrode impedance during subsequent high voltage, transvenous, sequential pulse shocks. Two transvenous defibrillation catheters were inserted in 15 patients undergoing electrophysiology study for the evaluation of ventricular tachycardia/fibrillation. A sequential pulse test shock at stored voltage of 50 or 100 volts was delivered during sinus rhythm and high voltage therapeutic shocks were delivered during induced ventricular tachycardia/fibrillation. The test shocks were well tolerated and caused only minimal discomfort. Peak delivered voltage for each pulse of the test shock ranged from 34 to 116 volts (mean 62 +/- 27) and for each pulse of the therapeutic shocks from 186 to 778 volts (mean 435 +/- 146). There was a very strong relationship between the impedance of the test and the mean impedance of the therapeutic shocks (R = 0.89, P less than 0.001). The mean impedance of the test shock was slightly greater than the mean impedance of the test shock as slightly greater than the mean impedance of the therapeutic shocks (mean 90 +/- 24 ohms compared to 77 +/- 16 ohms, P less than 0.001), with a maximum difference between test and therapeutic shock impedances of 39 ohms (mean difference 8.4 +/- 10.3 ohms). There was a significant inverse relationship between impedance and peak current (R = -0.49, P = 0.001). Cardiac and electrode impedance during transvenous defibrillation can be predicted reliably and safely by a low voltage test shock. This technique provides a safe and simple method to ensure appropriate connections and electrode function for subsequent countershock therapies.

The purpose of this study was to examine the effects of: (1) time to defibrillation and (2) subthreshold preshocks on defibrillation success. We conducted two separate experiments in 19 anaesthetized, open-chested pigs. Defibrillation was attempted using the sequential pulse technique approximately 10 s after electrically induced ventricular fibrillation. Each sequential pulse shock consisted of two trapezoidal pulses (approximately 3 ms duration), separated by 0.2 ms. Current was delivered to three mesh electrodes (TX-7, Medtronic) sutured over the anterior right ventricle, posterior right ventricle, and lateral left ventricle. For each animal, defibrillation threshold (DFT) defined as the lowest delivered energy that defibrillated the heart, was measured twice and the average was designated as mean DFT. The energy at 1.4 times the specific mean DFT for each pig was designated as the test shock and 100 volts less than the mean DFT was designated as the preshock. In the first experiment, test shocks were delivered at five different fibrillation intervals (10, 20, 40, 60, and 90 s). Time to test shock delivery was randomized for 10 to 60 s, but, 90 s was always tested at the end of the study. Percentages of success at 10, 20, 40, 60, and 90 s were 94, 78, 94, 83, and 100%, respectively (p = NS). The 12 pigs in which all initial test shocks were successful were selected for the evaluation of post defibrillation arrhythmias. The cumulative incidence of complete heart block lasting at least 5 s were 8, 33, 83, 83, and 83%, respectively. The incidence of complete heart block increased significantly at 40 s (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of myocardial ischemia on defibrillation success was studied using two different lead orientations in halothane-anesthetized pigs. Ischemia was induced by ligating the left anterior descending artery in its distal third. Controls had loosely tied ligatures placed around the artery at the same site. Ventricular fibrillation was induced by electrical stimulation 30 minutes after coronary artery ligation. Defibrillation used a single truncated pulse of approximately 6 ms duration passed to either: (1) a transvenous electrode catheter (Medtronic, 6880) with the cathode in the apex of the right ventricle and the anode in the superior vena cava-atrial junction region. or (21) the cathode in the apex of the right ventricle and a mesh plaque on the epicardium of the basal lateral left ventricle as anode. Ten seconds after the onset of ventricular fibrillation, defibrillation was attempted with increasing incremental energies until defibrillation was achieved. Fibrillation episodes were repeated at 15-minute intervals until the minimum first shock was successful in defibrillating the animal (i.e., defibrillation threshold). The number of animals successfully defibrillated with a minimum energy above or below 30 J was not different between normal and ischemic animals for either electrode configuration (i.e., 3 out of 20 vs 1 out of 13 for the catheter and 5 out of 6 vs 6 out of 7 for the epicardial plaque, respectively). Also, the cumulative percent success as a function of defibrillation energy was similar in both the normal and ischemic groups. There was a significant reduction in the minimum energy necessary for defibrillation when passing current between the right ventricular apex and the left ventricular epicardial plaque. The present results indicate that, despite differences in lead orientations, acute ischemia in the anesthetized pig does not appear to influence defibrillation success.

We evaluated the feasibility, safety, and efficacy of sequential pulse countershock (SqCS) delivered solely through two endocardial catheters for the termination of ventricular tachycardia (VT) and fibrillation (VF) in patients undergoing electrophysiology studies (EPS). Thirty-four patients (31 men, 3 women) with a mean age of 56.8 +/- 10.1 years were studied. Etiology of VT/VF was ischemic heart disease (n = 26), cardiomyopathy (4) repaired tetralogy of Fallot (n = 1), heart transplant (n = 1), and no identifiable heart disease (n = 2). Catheters were positioned successfully in 29 patients. These were positioned in the right ventricular apex (RVA) and the coronary sinus (CS), respectively. The RVA electrode served as the common cathode for both pulses. The two electrodes located near the right atrium/superior vena cava junction served as anode for pulse 1 while the distal CS electrodes served as anode for pulse 2. Twenty-nine induced VT episodes with cycle length (CL) 220-370 msec were treated. SqCS successfully terminated 15 VT (100-500V) while 14 were accelerated or degenerated to VF. VTCL was longer in successful SqCS episodes than in those that were accelerated (285 +/- 17.3 vs 245 +/- 30.8 msec, P less than .003). Of 26 VF episodes, 21 were terminated with SqCS (500-900V) and 5 were terminated by transthoracic rescue shocks. On 2 occasions, failure to defibrillate was attributable to poor catheter position at the time of shock. No complications occurred. We conclude that SqCS delivered solely between endocardial catheter electrodes is feasible and effective using energy doses within the range of existing implantable cardioverter defibrillators.

It has recently been shown that the probability of successful defibrillation as a function of energy has a sigmoidal dose-response relationship. Determination of a defibrillation "dose-response curve" is time consuming and requires multiple defibrillation attempts. On the other hand, determination of a defibrillation threshold is achieved rapidly and would be better suited to study the effect of interventions on the ability to defibrillate patients. We assessed the relationship of defibrillation threshold to the defibrillation "dose-response curve" in twelve open chest, halothane anesthetized pigs. Ventricular fibrillation was induced electrically, and defibrillation was attempted by passing sequential pulse shocks through an indwelling catheter and plaque electrodes. Defibrillation threshold was determined by decreasing the stored voltage of the initial shock until it failed to defibrillate the heart. Five different stored voltage levels distributed around defibrillation threshold were then randomly administered, six times for each level. A "dose-response curve" was obtained for each animal. Defibrillation threshold superimposed on the "dose-response curve" at 76 +/- 7.2 percent (mean +/- SEM) defibrillation success. Energy delivered at 1.5 times average defibrillation threshold was predicted to achieve 100 percent defibrillation success for a single shock in all animals. We conclude that defibrillation threshold provides a simple and quantitative estimate of the ability to defibrillate with a predictable relationship to the "dose-response curve."