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PubMed1981

Lidocaine in prehospital countershock refractory ventricular fibrillation.

Drug management of out-of-hospital countershock refractory ventricular fibrillation was evaluated by including 100 mg lidocaine bolus intravenously as the only anti-arrhythmic option in a protocol for use by paramedics. One hundred sixteen patients entered the study by failing to convert from ventricular fibrillation after the sequence of countershock, sodium bicarbonate, and repeat countershock. Sixty-two patients (53%) received lidocaine during the course of attempted resuscitation (Group I); 54 patients (47%) did not receive lidocaine (Group II). The two groups did not have significant differences in response times, patient profiles, or the use of other drugs or procedures. In Group I, 28 patients (45%) remained in ventricular fibrillation on arrival at the hospital, 15 (24%) were admitted to the CCU, and seven (11%) were ultimately discharged. In Group II, 25 patients (46%) remained in ventricular fibrillation on arrival at the hospital, eight (17%) survived to be admitted to the hospital, and one (2%) was ultimately discharged. The ability to convert ventricular fibrillation and the number of short- and long-term survivors did not differ significantly between the two groups. We conclude that a well-documented, controlled study of prehospital drug management of ventricular fibrillation is possible, and that further clinical evaluation of drug use in countershock refractory ventricular fibrillation is needed.

Anti-Arrhythmia Agents↗

PubMed1987

Effect of calcium-binding additives on ventricular fibrillation and repolarization changes during coronary angiography.

Ventricular fibrillation during coronary angiography with Renografin-76 (meglumine sodium diatrizoate) has been attributed to the calcium-binding additives sodium citrate and sodium ethylenediaminetetraacetic acid (EDTA), which may produce repolarization changes manifested as prolongation of the QT interval. Angiovist-370 is a newer form of meglumine sodium diatrizoate that contains calcium EDTA as its additive and thus has a decreased calcium-binding effect. Eight hundred sixteen patients were prospectively randomized to receive either Renografin-76 or Angiovist-370. Ventricular fibrillation occurred in 10 of 410 patients receiving Renografin-76 and in 0 of 406 patients given Angiovist-370 (p less than 0.0005). Clinical data were analyzed without knowledge of other data in the 10 patients treated with Renografin-76 who had ventricular fibrillation (Group I), 103 randomly selected patients who also received Renografin-76 but had no ventricular fibrillation (Group II) and 108 randomly selected patients given Angiovist-370 (Group III). Of several variables examined, only the QT interval differentiated patients receiving Renografin-76 and Angiovist-370. The mean corrected QT interval (QTc interval) before coronary angiography was slightly but not significantly (p = 0.7) higher in Group I than in Groups II and III. Ten seconds after the first left coronary artery injection it was more prolonged in Groups I and II (0.552 and 0.561 second, respectively) than in Group III (0.448 second) (p less than 0.00005). Similarly, 10 seconds after the first right coronary artery injection it was significantly longer in Groups I and II (0.545 and 0.544 second) than in Group III (0.477 second) (p less than 0.00005).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗

PubMed1989

Primary ventricular fibrillation in acute myocardial infarction.

Primary ventricular fibrillation is an acute life-threatening event if not treated promptly. The ability to predict this event during the course of an acute myocardial infarction could therefore have an important impact on the mode of treatment and monitoring. In the present study, clinical and laboratory information available at the initial evaluation of patients with an acute myocardial infarction was tested for its ability to predict subsequent primary ventricular fibrillation. Multiple logistic regression analysis was employed to select the predictors. Serum potassium, serum creatinine and no smoking were significant predictors of subsequent ventricular fibrillation. Although the prediction was statistically significant, the clinical value of the prediction is quite limited.

Aged↗

PubMed1976

Effect of nitroglycerin on ventricular fibrillation threshold of nonischemic myocardium.

The threshold for ventricular fibrillation induced by a 200 msec train of pulses was measured during a control period and during an intravenous infusion of nitroglycerin in 14 nonischemic open chest dogs. Infusion of nitroglycerin in doses sufficient to reduce mean arterial blood pressure an average of 17 mm Hg was associated with a rise in ventricular fibrillation threshold from a control value of 24 +/- 3 (mean +/- 1 standard error of the mean) to 41 +/- 6 milliamperes (P less than 0.001). In a subgroup of six animals simultaneous infusions of nitroglycerin and phenylephrine abolished the hypotensive effect of nitroglycerin but did not significantly alter the rise in ventricular fibrillation threshold observed with nitroglycerin infusion alone. In five other animals mean arterial blood pressure was similarly reduced an average of 17 mm Hg by venous hemorrhage, but was associated with a lowering than a rise in ventricular fibrillation threshold from a prehemorrhage value of 28 +/- 6 to 15 +/- 2 milliamperes, (P less than 0.005). Thus, intravenously administered nitroglycerin raises ventricular fibrillation threshold in nonischemic canine myocardium independent of its hypotensive effects.

Action Potentials↗

PubMed2003

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.

Animals↗

PubMed1996

Idiopathic ventricular fibrillation initiated by a short-coupled ventricular premature beat.

We report the case of a 38-year-old man who had idiopathic ventricular fibrillation (VF) which initiated by abnormally short-coupled ventricular premature beats. VF was successfully prevented by the combination of pilsicainide, propranolol, and verapamil. In particular, the effects of pilsicainide are assumed to exert an important effect in controlling this arrhythmia. Class Ic drugs may be effective for preventing VF initiated by short-coupled VPBs.

Adult↗

PubMed1983

Direct mechanical ventricular assistance during ventricular fibrillation.

A technique of direct mechanical ventricular assistance (DMVA) has been available since 1966. Ventricular assistance is provided by a glass cup lined with a Silastic diaphragm. It is held on the cardiac ventricles by suction. Alternating positive and negative pressure in the space between the cup and the diaphragm provides a pumping mechanism for blood flow. DMVA was compared to closed chest massage (CCM) and open chest massage (OCM) during ventricular fibrillation in six dogs. Each technique was applied for 10 minutes. Three dogs had CCM followed by OCM and then DMVA. Three dogs had only OCM and DMVA. Blood pressure and cardiac output were measured. All variables were calculated as a percentage of pre-ventricular-fibrillation values. Mean blood pressure was 19.7% with CCM, 39.8% with OCM, and 55.1% with DMVA. Systolic blood pressure was 25.8% with CCM, 51.9% with OCM, and 64.0% with DMVA. Diastolic blood pressure was 17.3% with CCM, 37.3% with OCM, and 48.9% with DMVA. Cardiac output was 13.8% with CCM, 37.1% with OCM, and 58.0% with DMVA. For each variable, OCM produced statistically higher values than did CCM. DMVA produced statistically higher values than did OCM for all variables. These preliminary results suggest that DMVA may be superior to currently available methods of cardiac massage during ventricular fibrillation.

Animals↗

PubMed1991

Determinants of successful transthoracic defibrillation and outcome in ventricular fibrillation.

OBJECTIVE: To examine factors determining defibrillation success and outcome in patients with ventricular fibrillation. DESIGN: Observational prospective study of age, sex, transthoracic impedance, site of cardiac arrest, ventricular fibrillation duration and amplitude, primary or secondary ventricular fibrillation, aetiology, number of shocks to correct ventricular fibrillation, and drug treatment. SETTING: A teaching hospital and a mobile coronary care unit with a physician. PATIENTS: 70 consecutive patients (50 male, 20 female) mean age 66.5 years. INTERVENTIONS: Before the first countershock was administered transthoracic impedance using a 30 kHz low amplitude AC current passed through 8 cm/12 cm self-adhesive defibrillator electrode pads applied in the anteroapical position was measured. The first two shocks were 200 J delivered energy (low energy) and further shocks of 360 J (high energy) were given if required. MAIN OUTCOME MEASURES: Countershock success and outcome from ventricular fibrillation. RESULTS AND CONCLUSIONS: First shock success was significantly greater in inhospital arrests (37/53) than in out-of-hospital arrests (5/17) and in those receiving antiarrhythmic treatment (13/15, 86.7%) v (27/51, 52.9%). Transthoracic impedance was similar in those who were successfully defibrillated with one or two 200 J shocks (98.7 (26) omega) and those who required one or more 360 J shocks (91.4 (23) omega). Success rates with two 200 J shocks were similar in those patients with "high" transthoracic impedance (that is, greater than 115 omega) and those with transthoracic impedance (less than or equal to 115 omega) (8/12 (67%) v 44/58 (76%]. Fine ventricular fibrillation was significantly more common in the patients with a transthoracic impedance of greater than 95 omega (41% (13/32] than in those with a transthoracic impedance less than or equal to 95 omega (13% (5/38]. Death during arrest was significantly more common in patients who needed high energy shocks (14/18 (78%] than in those who needed low energy shocks (16/52 (31%]. Multiple regression analysis identified ventricular fibrillation with an amplitude of greater than or equal to 0.5 mV, age less than or equal to 70 years, and arrests that needed less than or equal to two shocks for defibrillation, in rank order as independent predictors of survival to discharge.

Aged↗

PubMed1983

Ventricular fibrillation in acute myocardial infarction.

Ventricular fibrillation (VF) developed in 7.42% patients with acute myocardial infarction (AMI). It was more frequent among patients with anterior myocardial infarction compared to inferior myocardial infarction. On the basis of sequence of events, cases of ventricular fibrillation (VF) were classified in to Primary (P), Secondary (S) and Agonal (A). 57.69% cases had SVF, 30.76% had AVF and only 11.53% cases had PVF. In all cases of PVF, ECG was normal prior to the development of VF and developed abruptly without any warning.

Adult↗

PubMed1998

Phase angle convergence of multiple monophasic action potential recordings precedes spontaneous termination of ventricular fibrillation.

AIMS: To elucidate the mechanism of spontaneous termination of ventricular fibrillation (VF) and to define an indicator of its occurrence, the phase angle, a novel measure to assess synchrony of activation, was evaluated. METHODS AND RESULTS: In 7 isolated rabbit hearts, 7 monophasic action potentials were recorded simultaneously. Ventricular fibrillation was induced by T wave shocks. Cycle lengths (CL) and phase angles between all 7 recordings were analyzed until spontaneous termination or shock-induced defibrillation. Average phase angle was calculated as activation time difference to a reference channel and expressed as a fraction of the reference channel's CL with 1 equaling a complete CL. Initial CLs and phase angles were similar in sustained and terminating episodes (CL: 141 +/- 16 ms vs 142 +/- 24 ms, phase angle: 0.244 +/- 0.11 vs 0.263 +/- 0.1, p = NS). During spontaneous termination, CL increased slightly by 7%. Average phase angle converged gradually over the last three activations before termination of ventricular fibrillation by 22-48% (p < 0.0005), eventually resulting in phase angles similar to paced rhythms directly prior to spontaneous termination of ventricular fibrillation. CONCLUSIONS: Gradual synchronization of activation is part of the electrophysiological mechanism resulting in spontaneous ventricular fibrillation termination and can be detected three activations before termination. Phase angle convergence may be useful to detect spontaneous termination of ventricular fibrillation.

Action Potentials↗

PubMed1992

Mortality within hospital after resuscitation from ventricular fibrillation outside hospital.

OBJECTIVE: To determine factors related to mortality within hospital after successful resuscitation from ventricular fibrillation outside hospital by a mobile coronary care unit manned by a physician. DESIGN: Retrospective review of records of patients resuscitated and admitted to hospital between 1 January 1966 and 31 December 1987. SETTING: Mobile coronary care unit, coronary care unit, and cardiology department. PATIENTS: 281 patients (227 male), aged 14-82 (mean 58) successfully resuscitated from ventricular fibrillation outside hospital of whom 182 (65%) developed ventricular fibrillation before the arrival of the mobile coronary care unit. The aetiology of ventricular fibrillation was acute myocardial infarction in 194 patients (69%), ischaemic heart disease without infarction in 71 (25%), and other or unknown in 16 (6%). MAIN OUTCOME MEASURES: Death within hospital. RESULTS: There were 91 deaths in hospital (32%). Factors on univariate analysis significantly associated with increased mortality were patient age > or = 60 years, previous myocardial infarction or cerebrovascular disease, prior digoxin or diuretic treatment, collapse without prior chest pain or with pain lasting 30 minutes or less, defibrillation delayed by > or = 5 min, > or = four shocks required to correct ventricular fibrillation, left ventricular failure or pulmonary oedema and cardiogenic shock after successful defibrillation, and coma on admission to hospital. On multivariate analysis the most important factors (in rank order) were cardiogenic shock after defibrillation, coma on admission to hospital, age > or = 60 years and the requirement for four or more shocks to correct ventricular fibrillation. CONCLUSIONS: The in-hospital mortality of patients resuscitated from ventricular fibrillation outside hospital was related to patient characteristics before the cardiac arrest and to the immediate haemodynamic and neurological status after correction of ventricular fibrillation as well as to factors at the resuscitation itself. The in-hospital mortality of this study compares favourably with the results obtained by units staffed by paramedical workers and emergency medical technicians, although 35% (99/281) of the patients had ventricular fibrillation after the arrival of the mobile unit and defibrillation was thus rapid.

Adult↗

PubMed1996

Drifting vortices of electrical waves underlie ventricular fibrillation in the rabbit heart.

Ventricular fibrillation is the most important cause of cardiac electrical instability leading to sudden death. Fibrillation is believed to be associated with complex three-dimensional (3-D) spatio-temporal patterns of electrical excitation of the myocardium. However, to this date, such patterns have not been directly observed or characterized, and little is known about their dynamics. In this paper, we present results that strongly support the hypothesis that at least some cases of ventricular fibrillation in the structurally normal heart may be the result of a single 3-D electrical scroll wave that moves rapidly throughout the ventricles, giving rise to complex patterns of cardiac muscle excitation.

Animals↗

PubMed1995

Role of intracellular calcium in the antiarrhythmic effect of procainamide during ventricular fibrillation in rat hearts.

Increased intracellular calcium (calcium overload) is considered one of the factors that can initiate ventricular fibrillation. In addition, ventricular fibrillation itself can cause and possibly maintain calcium overload. The goal of this study was to determine whether the class IA antiarrhythmic agent procainamide can reduce calcium overload during ventricular fibrillation and, if so, whether this reduction could be responsible for the recovery of the left ventricular function after defibrillation. For this purpose, the effects of 0.1 mmol/L of procainamide perfusion on left ventricular developed pressure, cardiac rate, and intracellular calcium during pacing-induced ventricular fibrillation were measured in isolated perfused rat hearts. Intracellular calcium was assessed by surface fluorometry after indo 1 loading. The concentration of procainamide was selected such that approximately half of the hearts would functionally recover from fibrillation. Cardiac rate and intracellular calcium were compared among four groups, depending on both the perfusate used and the recovery of left ventricular developed pressure at the end of the experiment. We found that procainamide reduced intracellular calcium to steady-state levels in hearts in which left ventricular function completely recovered (developed pressure > 67% of the steady-state value). However, intracellular calcium remained elevated in partially recovered hearts (33% < or = pressure < or = 67%) and in nonrecovered hearts (pressure < 33%). Thus procainamide can reduce calcium overload during ventricular fibrillation, and this reduction could be responsible for the recovery of left ventricular function after defibrillation. This reduction was use dependent, that is, dependent on high cardiac rates during fibrillation rather than on the decrease of cardiac rates before or during defibrillation.

Analysis of Variance↗

PubMed1990

Preservation of ventricular function by treatment of ventricular fibrillation with phenylephrine.

Epinephrine promotes resuscitation from ventricular fibrillation because of its peripheral vasoconstrictive effects. However, the beta-adrenergic effects of epinephrine may be detrimental because of the stimulation of myocardial oxygen demand. To test whether functional recovery from fibrillation in hearts treated with a selective alpha-adrenergic agent is greater than in hearts treated with epinephrine, ventricular fibrillation was induced in eight isolated dog hearts while coronary perfusion pressure was maintained at 30 mm Hg. In random order, epinephrine (5 micrograms/min), phenylephrine (50 micrograms/min) or no drug was infused for 5 min. The heart was then defibrillated, the drug infusion stopped and coronary perfusion pressure increased to 100 mm Hg. Coronary blood flow (ml/min per 100 g), arteriovenous oxygen difference (ml O2/dl) and myocardial oxygen consumption (ml O2/min per 100 g) measured after 4 min of ventricular fibrillation were greater with epinephrine (mean +/- SD 30.9 +/- 11.7, 17.5 +/- 1.6 and 5.4 +/- 1.9, respectively) than with phenylephrine (24.4 +/- 6.0, 15.7 +/- 2.6 and 3.8 +/- 1.1, respectively) or no drug (19.8 +/- 5.2, 12.8 +/- 1.8 and 2.6 +/- 0.7, respectively) (p less than 0.05, p less than 0.05 and p less than 0.05, respectively). The slope of the end-systolic pressure-volume relation 10 min after defibrillation and restoration of normal coronary perfusion pressure was depressed (percent of prefibrillation value) most by epinephrine infusion (72 +/- 17%, n = 6), less by no drug infusion (82 +/- 12%, n = 4) and was increased after phenylephrine infusion (143 +/- 17%, n = 6) (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Sixty-six episodes of ventricular fibrillation within four hours: electrical stability restored by propafenone.

Ventricular fibrillation is a complication in patients hospitalized for acute myocardial infarction. We report the case of an unusually high number of episodes of ventricular fibrillation (66 episodes) that occurred within a period of 4 h in a patient with recent anterior myocardial infarction. In patients with acute or recent myocardial infarction and recurrent episodes of ventricular fibrillation, intravenous lidocaine is the antiarrhythmic medication of choice. In our patient, recurrences of ventricular fibrillation were not prevented either by lidocaine, or amiodarone. The rate of recurrence of ventricular fibrillation, however, decreased dramatically, twice, in the minutes following two separate boluses of propafenone, and the arrhythmia did not recur when continuous infusion of propafenone was started. We cannot exclude that were the combined antiarrhythmic effects of lidocaine, amiodarone and propafenone that led to the final control of the arrhythmia.

Amiodarone↗

PubMed1995

Analysis of the body surface ECG measured in independent leads during ventricular fibrillation in humans.

The degree of myocardial electrical organization during ventricular fibrillation remains unknown. The aim of this study was to compare the characteristics of the surface ECG on three independent and approximately orthogonal leads. Ten recordings of ventricular fibrillation, each induced at electrophysiology study and successfully terminated by direct current shock, were analyzed. Each recording was divided into 1-second epochs for analysis. Frequency analysis using the Fast Fourier Transform showed that the frequency of the dominant spectral peak increased significantly from a mean of 4.1 +/- 0.8 Hz to 5.2 +/- 0.7 Hz during the first 5 seconds of ventricular fibrillation. In 95% of the epochs analyzed, a similar dominant frequency was observed on either two or three ECG leads. Frequency agreement tended to increase as ventricular fibrillation evolved. This study shows that the rate of ventricular fibrillation increases rapidly during the first 5 seconds but only gradually thereafter, and that similar signal characteristics are observed on independent ECG leads. These findings are not compatible with the traditional view of incoherent myocardial activity during ventricular fibrillation.

Body Surface Potential Mapping↗

PubMed2001

Effects of biphasic vs monophasic defibrillation on the scaling exponent in a swine model of prolonged ventricular fibrillation.

OBJECTIVE: Mathematical analyses of ventricular fibrillation (VF) have resulted in the derivation of a measure termed the scaling exponent (ScE) that characterizes the duration of VF and probability of defibrillation success. The purpose of this study was to compare the effects of biphasic defibrillation waveform (BDW) and monophasic defibrillation waveform (MDW) rescue shocks on ScE in a swine model of prolonged VF. METHODS: Utstein guidelines for the laboratory study of cardiopulmonary resuscitation were followed. Twenty mixed-breed domestic swine (mass range 20.5-26.8 kg) were instrumented and randomized to receive either MDW or BDW rescue shocks. Ventricular fibrillation was induced and untreated for a nonintervention interval of 8 minutes. Rescue shocks were delivered at 8, 10, and 12 minutes of elapsed VF time. The energy sequence for the three MDW shocks was 70, 100, and 150 J (approximately 3, 4, and 6 J/kg). All BDW shocks were delivered at 50 J (approximately 2.5 J/kg). Only VF was shocked. Chest compressions and drugs were not provided. Rhythm analysis and ScE calculation were performed offline. Continuous and discontinuous linear regression models were fit to plots of ScE vs time. Defibrillation success and progression of ScE slope were analyzed using Fisher's exact test, paired t-tests, and repeated-measures analysis of variance (ANOVA). RESULTS: Baseline characteristics were similar for both groups. Successful termination of VF occurred on the first rescue shock in 1 of 10 (10%) in the MDW group and 3 of 10 (30%) in the BDW group; this difference was not statistically significant (p = 0.58). No other defibrillation successes were observed. No animals achieved return of spontaneous circulation. The ScE values during the protocol progressed from 1.330 (95% CI = 1.287 to 1.373) to 1.724 (95% CI = 1.603 to 1.845) for MDW and 1.338 (95% CI = 1.261 to 1.415) to 1.639 (95% CI = 1.530 to 1.745) for BDW. Both groups showed a trend toward increasing ScE values with successive rescue shocks. Repeated-measures ANOVA using both continuous and discontinuous models demonstrated no difference in overall ScE slope progression between study groups. CONCLUSIONS: Mode of defibrillation waveform (BDW vs MDW) does not appear to impact ScE trends. Additional studies must be performed to better evaluate the clinical implications of this finding.

Animals↗

PubMed2000

Distribution of excitation frequencies on the epicardial and endocardial surfaces of fibrillating ventricular wall of the sheep heart.

Tissue heterogeneities may play an important role in the mechanism of ventricular tachycardia (VT) and fibrillation (VF) and can lead to a complex spatial distribution of excitation frequencies. Here we used optical mapping and Fourier analysis to determine the distribution of excitation frequencies in >20 000 sites of fibrillating ventricular tissue. Our objective was to use such a distribution as a tool to quantify the degree of organization during VF. Fourteen episodes of VT/VF were induced via rapid pacing in 9 isolated, coronary perfused, and superfused sheep ventricular slabs (3x3 cm(2)). A dual-camera video-imaging system was used for simultaneous optical recordings from the entire epi- and endocardial surfaces. The local frequencies of excitation were determined at each pixel and displayed as dominant frequency (DF) maps. A typical DF map consisted of several (8.2+/-3.6) discrete areas (domains) with a uniform DF within each domain. The DFs in adjacent domains were often in 1:2, 3:4, or 4:5 ratios, which was shown to be a result of an intermittent Wenckebach-like conduction block at the domain boundaries. The domain patterns were relatively stable and could persist from several seconds to several minutes. The complexity in the organization of the domains, the number of domains, and the dispersion of frequencies increased with the rate of the arrhythmia. Domain patterns on the epicardial and endocardial surfaces were not correlated. Sustained epicardial or endocardial reentry was observed in only 3 episodes. Observed frequency patterns during VT/VF suggest that the underlying mechanism may be a sustained intramural reentrant source interacting with tissue heterogeneities.

Animals↗