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PubMed1994

Evoked potential monitoring during repeatedly induced ventricular fibrillation for internal defibrillator implantation.

Repeated induction of ventricular fibrillation (VF) with circulatory compromise during implantable cardioverter defibrillator (ICD) testing may cause cerebral injury. To test this hypothesis, somatosensory evoked potentials (SEP), a more sensitive marker of injury, were recorded in patients (N = 10) undergoing ICD implantation. SEP were recorded before induction of anesthesia, after induction of anesthesia, before and at several times following induction of VF. Possible modifying factors of the SEP measurements such as anesthetic application, blood pressure, body temperature, and hematocrit remained constant throughout the operations. Central conduction time was unaffected by ICD defibrillation testing. Amplitude of SEP primary complexes was transiently reduced at 34.9% (P < 0.01) by defibrillation testing, but returned to control within 10 minutes after testing. It is concluded that while ICD defibrillation testing may produce transient changes in SEP, there is no evidence of residual cerebral injury.

Adult↗

PubMed2003

Spatial distribution of phase singularities in ventricular fibrillation.

BACKGROUND: Multiple excitation wavelets are present during ventricular fibrillation (VF). The underlying wavelet organization of VF is unclear. Phase singularities (PSs)-locations of ambiguous activation state-underlie reentry and wavelet splitting and represent the sources of VF. Understanding the mechanisms of PS formation might be important in the development of effective therapies for sudden death. METHODS AND RESULTS: We performed voltage, phase, and PS mapping in fibrillating ventricles, applying an automated PS detection algorithm to optically recorded fibrillation signals. PS clustering was noted along epicardial vessels, ridges of endocardial trabeculae, and papillary muscle insertions. Microscopically, these locations correlated with areas of apposition of fibers with different angulations and intramural vessels. A total of 83.2% of PSs were formed at and meandered about these anatomic structures, which acted as stabilizers: PSs colocalizing at anatomic substrates had longer life spans than nonanatomic PS (82.46+/-60.8 versus 40.5+/-31.9 ms, P<0.01). The RV endocardium had a higher PS incidence than the epicardium (42.3+/-9.2 versus 23.5+/-11.6 PS/s, P<0.01). Autocorrelation showed that irregular behavior was spatially restricted to anatomic heterogeneities compared with other areas, which had nearly periodic behaviors. Simple spatial PS distributions underlay complex and variable activation patterns attributable to variable PS behaviors, life spans, and inter-PS interactions. CONCLUSIONS: PSs occur in a nonrandom spatial distribution and colocalize with normal anatomic heterogeneities. Varying PS behaviors and life spans but stable PS spatial distributions cause ever-changing activation patterns that characterize VF.

Animals↗

PubMed1984

Correlates of reperfusion ventricular fibrillation in dogs.

To elucidate determinants of reperfusion ventricular fibrillation (VF), regional myocardial blood flow, ATP, creatine phosphate (CP), heart rate and blood pressure were compared in 2 groups of anesthetized dogs: those that fibrillated spontaneously upon release of a 15-minute coronary artery occlusion (VF group, n = 8) and those that did not fibrillate when reperfused (No VF group, n = 27). Arterial pressure and heart rate before and during coronary artery occlusion were similar in both groups. Ischemic endo- and epicardial ATP values, measured at the end of the occlusion period, were reduced approximately 20% of nonischemic values in both groups. In contrast, CP (nmol . mg protein-1) within the ischemic zone was significantly lower in the VF group in both the epicardium (14.3 +/- 1.6 in the VF group vs 22.8 +/- 2.5 in the No VF group, p less than 0.01) and the endocardium (9.0 +/- 2.0 in the VF group vs 18.7 +/- 1.8 in the No VF group, p less than 0.01). Furthermore, epi- and endocardial regional myocardial blood flow in the center of the ischemic zone during occlusion was significantly lower in VF dogs than in No VF dogs. Epicardial flow was 0.06 +/- 0.03 ml X min-1 X g-1 in VF dogs vs 0.44 +/- 0.06 in No VF dogs (p less than 0.001) and endocardial flow was 0.03 +/- 0.02 ml X min-1 X g-1 in VF dogs vs 0.23 +/- 0.04 ml X min-1 X g-1 in No VF dogs (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1993

A reappraisal of ventricular fibrillation threshold testing.

To test the hypothesis that ventricular fibrillation (VF) threshold testing is a probability function, 12 open-chest dogs were studied. The VF thresholds were tested by scanning the T wave with either the single premature stimulus method or with the train stimulus method. The dose-response curve method was used to determine the probability of inducing VF with different strengths of premature stimulation. Conventional methods and up-down methods were also used to test the VF threshold. The results showed that the VF threshold is a probability function. The conventional method VF threshold for the single premature stimulus and for the train stimulus methods corresponded to the current strength associated with a 23.4 +/- 13.2 and a 33.2 +/- 19.5% probability of VF (P < 0.05), respectively. In comparison, the triplicate VF threshold determined by the up-down algorithm method resulted in values that were not significantly different from a 50% probability of inducing VF, with a good correlation (r = 0.90, P < 0.001 for single and r = 0.89, P = 0.003 for the train stimulus method). We conclude that: 1) The VF threshold is a probability function, and 2) the triplicate VF threshold determined by the up-down algorithm method is the best alternative to the dose-response curve method in estimating 50% probability of inducing VF.

Algorithms↗

PubMed1992

Deterioration of ventricular tachycardia to ventricular fibrillation after rapid intravenous administration of magnesium sulfate.

We report the case of a patient who had development of ventricular fibrillation following rapid intravenous administration of magnesium sulfate (2 g over 5 s) for treatment of sustained monomorphic ventricular tachycardia. Initial slowing of the tachycardia was followed by gradual widening of QRS complexes and electrical alternans, leading to ventricular fibrillation within 3 min of magnesium administration.

Aged↗

PubMed1988

Effect of esmolol on the ventricular fibrillation threshold.

The effect of esmolol on the ventricular fibrillation threshold (VFT) was determined in 11 open-chest dogs anesthetized with sodium pentobarbital. Since changes in VFT by antiarrhythmic drugs have been shown to depend on the method used to test vulnerability to fibrillation, two methods were studied. The vulnerable period was scanned with a train of pulses (100 Hz, 4 ms, 20 pulses) in nine experiments and a single pulse (10 ms) in eight experiments. Following control measurements, esmolol was administered as an intravenous bolus of 500 micrograms/kg followed by a continuous infusion of 300 micrograms/kg/min. After 15 min of infusion, the adequacy of beta-blockade was tested by the administration of 0.5 micrograms/kg of isoproterenol. Isoproterenol increased the heart rate by only 18 +/- 2 beats/min following esmolol administration which was significantly less than the control response (79 +/- 7 beats/min, p less than 0.01). Although the VFT measured with the single-pulse technique did not change in response to esmolol (14.1 +/- 1.1 mA vs. 14.3 +/- 1.2 mA), the VFT measured with the train-of-pulses technique significantly increased (3.7 +/- 0.5 mA to 14.5 +/- 2.8 mA, p less than 0.01). Twenty minutes after discontinuing esmolol, the VFT measurements were repeated and did not differ from control values with either technique. The increase in heart rate in response to isoproterenol also returned to control values (80 +/- 6 beats/min). The results suggest that the ability of esmolol to raise VFT as measured by the train-of-pulses technique is due to beta-adrenergic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed2006

Transthoracic incremental monophasic versus biphasic defibrillation by emergency responders (TIMBER): a randomized comparison of monophasic with biphasic waveform ascending energy defibrillation for the resuscitation of out-of-hospital cardiac arrest due to ventricular fibrillation.

BACKGROUND: Although biphasic, as compared with monophasic, waveform defibrillation for cardiac arrest is increasing in use and popularity, whether it is truly a more lifesaving waveform is unproven. METHODS AND RESULTS: Consecutive adults with nontraumatic out-of-hospital ventricular fibrillation cardiac arrest were randomly allocated to defibrillation according to the waveform from automated external defibrillators administered by prehospital medical providers. The primary event of interest was admission alive to the hospital. Secondary events included return of rhythm and circulation, survival, and neurological outcome. Providers were blinded to automated defibrillator waveform. Of 168 randomized patients, 80 (48%) and 68 (40%) consistently received only monophasic or biphasic waveform shocks, respectively, throughout resuscitation. The prevalence of ventricular fibrillation, asystole, or organized rhythms at 5, 10, or 20 seconds after each shock did not differ significantly between treatment groups. The proportion of patients admitted alive to the hospital was relatively high: 73% in monophasic and 76% in biphasic treatment groups (P=0.58). Several favorable trends were consistently associated with receipt of biphasic waveform shock, none of which reached statistical significance. Notably, 27 of 80 monophasic shock recipients (34%), compared with 28 of 68 biphasic shock recipients (41%), survived (P=0.35). Neurological outcome was similar in both treatment groups (P=0.4). Earlier administration of shock did not significantly alter the performance of one waveform relative to the other, nor did shock waveform predict any clinical outcome after multivariate adjustment. CONCLUSIONS: No statistically significant differences in outcome could be ascribed to use of one waveform over another when out-of-hospital ventricular fibrillation was treated.

Adult↗

PubMed1989

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold.

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.

Animals↗

PubMedDate not supplied

[Ventricular fibrillation in myocardial infarct patients: the factors determining the prognosis].

Improvement of methods for diagnosis and treatment of myocardial infarction and its complications permitted the mortality and disability resulting from this condition to be considerably reduced. The aim of the study was to analyse in retrospect clinical and functional disorders in subjects with a history of ventricular fibrillation in the acute phase. Over 3 years, 1096 patients with acute myocardial infarction had been admitted to the Department of Cardioresuscitation. Ventricular Fibrillation was cause of death in 2.1% of cases. Over this time period, resuscitation was a success in 2.9%. The following item was found out to be a factor of unfavourable prognosis during the first two years after development of acute myocardial infarction: it was postinfarction dilatation of the left ventricle having a part in the evolution of cardiac insufficiency and contributing to formation of arrhythmogenic substrate and, to a lesser degree, to ventricular fibrillation in the acute phase.

Cause of Death↗

PubMed1993

Effects of myocardial fiber orientation on the electrical induction of ventricular fibrillation.

Although many studies have documented the importance of myocardial fiber orientation in the generation and maintenance of reentrant arrhythmia, its role in the induction of reentry by a single strong premature stimulus is held to be minimal. To study the importance of fiber orientation on the mechanisms of ventricular vulnerability to single strong premature electrical stimulation, computerized mapping studies using 56 closely (2. 5-5 mm) spaced epicardial bipolar electrodes were performed on six open-chest dogs to determine the patterns of activation after the application of a single strong premature stimulus. In an additional three dogs, both epicardial and endocardial mapping studies were performed with closely spaced electrodes. The baseline driving stimulus (S1) and the premature stimulus (S2) were given to the same or different sites on the right ventricular epicardium. When the line connecting the S1 and S2 (the electrical axis of stimulation) was roughly parallel to the fiber orientation, the vast majority of the early sites were found to lie between the S1 and S2 sites, with none of the early sites occurring on the side of the S2 site opposite to the S1 site. At the onset of ventricular fibrillation, figure-eight reentry was easily demonstrated. In comparison, when the S1 and S2 were given to the same site, or when the electrical axis of stimulation was roughly perpendicular to the fiber orientation, the early sites could occur on all sides of the S2 site. In these instances, a figure-eight reentry was not present at the onset of ventricular fibrillation, although this pattern could develop after the first few beats. These findings indicate that myocardial fiber orientation is an important factor in determining the patterns of activation during the electrical induction of ventricular fibrillation.

Animals↗

PubMed2004

A 25-year control of idiopathic ventricular fibrillation with electrophysiologic-guided antiarrhythmic drug therapy.

The case of a 28-year-old man with recurrent syncope and multiple documented episodes of idiopathic ventricular fibrillation is reported. Recurrent syncope suggesting a self-terminating ventricular tachyarrhythmia occurred after 1 month of amiodarone therapy, and ventricular fibrillation was inducible at electrophysiologic study. After addition of quinidine, no significant ventricular arrhythmias could be induced. Similar results were found during a repeat electrophysiologic study performed 23.5 years later. During a 25-year period, the patient has remained arrhythmia-free on combined antiarrhythmic medication with quinidine and amiodarone.

Adult↗

PubMed1990

Cardiac resuscitability with cardiopulmonary bypass after increasing ventricular fibrillation times in dogs.

Previous studies in dogs have shown resuscitation from prolonged cardiac arrest to conscious survival to be more effective with the use of cardiopulmonary bypass (CPB) than with standard advanced cardiac life support. This study compared cardiovascular resuscitability with CPB only after varying periods of cardiac arrest without artificial circulatory support in a canine model. Group 1 (ten) was subjected to ventricular fibrillation for 15 minutes; group 2 (ten) for 20 minutes; and group 3 (ten) for 30 minutes. All received total CPB after ventricular fibrillation without advanced cardiac life support to defibrillation at two to five minutes and partial CPB to four hours. In all three groups CPB with epinephrine generated normal coronary perfusion pressure and increased ventricular fibrillation amplitude significantly. In groups 1 and 2, CPB reperfusion allowed for successful defibrillation in less than five minutes, weaning from CPB in all dogs at four hours, and stable spontaneous circulation thereafter. In group 3, only five of ten dogs could be weaned from bypass at four hours, and all died early with myocardial necroses. It was concluded that CPB may be of value in the setting of prolonged cardiac arrest when advanced cardiac life support has not been provided or is unable to restore spontaneous heart-beat.

Animals↗

PubMed1980

Amiodarone-induced ventricular fibrillation.

Amiodarone, 600 mg orally daily, was used in an attempt to control supraventricular tachyarrhythmias in a patient with the sick sinus syndrome. Twenty days from the onset of therapy the Q-T interval lengthened. Episodes of ventricular flutter, ventricular fibrillation and self-terminating ventricular tachyarrhythmia (torsade de pointes) developed on the 28th day of amiodarone therapy. Temporary cardiac pacing prevented further episodes of ventricular fibrillation. Despite the suggestion that this drug may be given in large doses for long periods of time since it has a wide safety margin, we feel that the risk of lethal arrhythmias is such that caution is required in its use.

Amiodarone↗

PubMed1976

Atrial rhythm during ventricular fibrillation in the dog.

Depolarization of the atrioventricular junctional tissues and of the atrial septum was examined in the perfused dog heart before and during ventricular fibrillation by (1) recording the potentials from the junctional tissues in the regions of the interatrial and interventricular septum and examining the relationship of activity at these sites to atrial depolarization, (2) computing histograms and autocorrelograms of atrial firing intervals to study atrial rhythmicity, and (3) plotting the sequence of atrial septal depolarization. The junctional tissue was generally randomly depolarized by the fibrillating ventricles. The histograms and autocorrelograms indicate that during ventricular fibrillation the atrial depolarization intervals do not remain constant, but vary widely. This seems to be due to the retrograde excitation from the junctional tissues. Plots of the depolarization sequences of the interatrial septum also indicate that retrograde depolarization takes place. The junctional tissues decrease the number of impulses that can pass from ventricle to atrium, and they similarly decrease the number of impulses that pass in an antegrade direction during atrial fibrillation.

Animals↗

PubMed1983

Spontaneous ventricular fibrillation occurring immediately after institution of cardiopulmonary bypass: possible clinical implications.

Twenty-four patients developed spontaneous ventricular fibrillation (SVF), for no apparent reasons, immediately after the institution of cardiopulmonary bypass (CPB) and prior to aortic cross-clamping and cardioplegic arrest. These were compared to 76 similar patients who remained in normal sinus rhythm (NSR). The following observations were made: (1) SVF occurred more frequently in patients undergoing urgent coronary bypass and having unstable or crescendo angina with severe triple coronary artery disease and/or left main coronary artery stenosis; (2) in nonvented hearts the mean left atrial pressure increased to levels above 28 mm Hg during SVF and prior to cardioplegic arrest; (3) at the end of CPB, arrhythmias and episodes of ventricular fibrillation were common (48% SVF versus 8% NSR); (4) the overall myocardial infarction rate was 37% SVF versus 4% NSR; and (5) the mortality rates were 25% SVF versus 1.3% NSR. It is postulated that the occurrence of SVF at the start of CPB may be indicative of serious derangements in myocardial cellular metabolism and/or function and may have clinical and prognostic implications.

Cardiopulmonary Bypass↗

PubMed1994

The value of electrophysiologic testing in patients resuscitated from documented ventricular fibrillation.

INTRODUCTION: Electrophysiologic testing is performed in patients resuscitated from ventricular fibrillation (VF) on the assumption that sustained monomorphic ventricular tachycardia (VT) may be a precursor to VF, with the former amenable to assessment by serial drug testing. METHODS AND RESULTS: We assessed the usefulness of this strategy by analyzing clinical and electrophysiologic data of 42 survivors (29 men and 13 women; mean age 54 +/- 14 years) of VF without a reversible cause. All patients had VF documented on ECG and required defibrillation. Underlying heart diseases included coronary disease in 28, dilated cardiomyopathy in 3, arrhythmogenic right ventricular dysplasia in 1, and no apparent structural heart disease in 10 patients. Only 2 (4.7%) patients had a prior history of documented VT. The electrophysiologic study was performed 7 to 30 days after VF. Programmed stimulation at the right ventricular apex using at least two drive cycle lengths and up to three extrastimuli induced sustained monomorphic VT in 4 (9.5%), sustained polymorphic VT in 3 (7.1%), nonsustained monomorphic VT in 1 (2.3%), nonsustained polymorphic VT in 5 (11.9%), and VF in 13 (30.9%) patients. Two patients with documented prior VT and coronary disease had sustained VT induced during the electrophysiologic study. On the other hand, sustained monomorphic VT was induced in 53 of the 59 (90%) patients (45 men and 14 women; mean age 57 +/- 16 years) with clinically documented VT concurrently studied using the same stimulation protocol. CONCLUSION: We conclude that reproducible induction of sustained monomorphic VT in survivors of documented VF is uncommon. It may be more cost effective to proceed directly to treatment with implantable cardioverter defibrillators in these patients.

Adult↗

PubMed1990

Changes in ventricular fibrillation threshold during the development of perinephritic hypertension.

Established hypertension is associated with enhanced susceptibility to life-threatening arrhythmias. However, little is known about the effects of the development of hypertension on the electro-physiological properties of the heart. To study this relationship, dogs were chronically instrumented for recording mean arterial pressure and conducting cardiac electrical testing during right ventricular pacing using an intracavitary bipolar catheter. In normotension, ventricular fibrillation threshold was determined under alpha-chloralose anesthesia, after which perinephritic hypertension was induced by wrapping one kidney in silk followed by contralateral nephrectomy. During serial testing of the same animals, ventricular fibrillation threshold was significantly increased early in the development of hypertension (2 to 3 weeks after renal wrapping), but found to be significantly reduced at 6 to 7 weeks after renal wrapping. The increase in ventricular fibrillation threshold was eliminated by cholinergic blockade.

Animals↗

PubMedDate not supplied

Transient giant R waves in the early phase of acute myocardial infarction: association with ventricular fibrillation.

An unusual electrocardiographic (ECG) pattern was observed in five patients who suffered an acute anterior myocardial infarction. Early in their illness and following resuscitation from ventricular fibrillation (three patients), in the midst of recurrent ventricular irritability prior to development of ventricular fibrillation (one patient), and following a period of seizures (one patient), the ECG showed ST-segment elevation, marked increase in the R-wave amplitude, disappearance of S waves and merging of QRS complexes with the elevated ST segments, ECG patterns noted in these patients were similar to the ones recorded from dogs immediately after ligation of a large coronary artery, and from patients with severe episodes of variant angina. Although these early electrocardiographic changes probably reflect either marked regional transmural blood flow deprivation or its aftermath, they could not be taken as indices of eventual massive myocardial necrosis since in most of these patients the alterations were followed by development of nontransmural myocardial infarction. The possible mechanisms and the implications of such discrepancy between early and late electrocardiographic indicators of injury or necrosis is discussed.

Adult↗