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PubMedDate not supplied

[Signaling indicator of ventricular fibrillation].

The purpose of the work was to design an appliance for reliable detection of ventricular fibrillation. Frequency-amplitude spectrum of electrocardiograms taken in dogs with normal rhythm and fibrillation, as well as the impulse ratio in normalcy, tachycardia and in fibrillation were investigated. An appliance for automatic separation of ventricular fibrillation by referring to pulse ratio is described. The designed device is shown to have a high degree of discrimination and noise-immunity.

Animals↗
PubMedDate not supplied

[Analysis of ECG in ventricular fibrillation in man and animals based on chaos theory].

The methods of the chaos theory were used to estimate the degree of irregularity of ventricular fibrillation in human and experimental animals. To verify the hypothesis that the degree of chaos depends on the species of the living organisms, the parameters characterizing the degrees of irregularity of ventricular fibrillation were estimated and compared. The comparative analysis was performed using 32 fragments of electrocardiographic records from five patients with sudden ventricular fibrillation bouts and 215 episodes of induced fibrillation in 17 animals. It was shown that fibrillation in human and animals has a different degree of regularity and different values of the chaotic component. The highest values of chaos were recorded in dogs, the lowest degree of chaos was observed in human. Rabbits and rats are intermediate, between dogs and humans. The fractuality of the structure-function organization of myocardium is discussed.

Animals↗
PubMedDate not supplied

The effect of heart rate on the termination of electrically induced ventricular fibrillation in the isolated perfused rat heart.

Ventricular fibrillation (VF) which is normally sustained in large animals and humans, is transient in small animals. The purpose of the present study was to evaluate the possible effect of changing cardiac rate on spontaneous ventricular defibrillation. In isolated perfused rat heart, VF was electrically induced during normal spontaneous rhythm of the heart at normal rate and at various ventricular pacing rates. It was found that: 1) Electrically induced VF in isolated perfused, non-ischemic rat heart spontaneously terminated in 88% of the hearts; 2) Ventricular pacing rhythm of spontaneous rate plus 10% caused VF to be sustained in 26% of the hearts (which defibrillated spontaneously during normal rates); 3) Ventricular pacing at 200% of the basic rate led to sustained VF in about half the VF episodes (14 out of 33, p less than 0.005). In the remainder, which defibrillated spontaneously, a sustained VF could be achieved by further increase in ventricular pacing rate; 4) Slow pacing rate, as a result of the surgical production of atrioventricular (A-V) block, enhanced the probability of spontaneous defibrillation (21 of 21 episodes after slow pacing vs 24 of 34 episodes following pacing at previous normal sinus rhythm, p less than 0.05). Selective modulation of conduction velocity, refractory period or both, achieved by changes in ventricular pacing rate was assumed to play an important role in determining whether electrically-induced VF would be transient or sustained.

Animals↗
PubMed2004

Fever as a precipitant of idiopathic ventricular fibrillation in patients with normal hearts.

INTRODUCTION: Ventricular fibrillation (VF) is the main mechanism of sudden cardiac death. The clinical precipitants of sudden cardiac death due to idiopathic VF are poorly characterized. Emerging evidence implicates triggers originating predominantly from the distal Purkinje arborization and the right ventricular outflow tract. METHODS AND RESULTS: We report three patients without structural heart disease or repolarization abnormalities in whom a febrile illness was the only concurrent disease associated with unexpected sudden cardiac death due to VF storm. An automated defibrillator was implanted in all three patients. In one patient with persistent recurrent VF episodes, mapping demonstrated the origin of these triggers was from the Purkinje arborization of the anterior wall of the right ventricle. Ablation at a site of earliest activation during ectopy, where pace mapping was concordant and Purkinje potential preceded the onset of ventriculogram, resulted in suppression of all arrhythmias. After follow-up of 22, 9, and 18 months in the three patients, no ventricular arrhythmias have been recorded. CONCLUSION: We present a series of patients in whom an apparently benign febrile illness was associated with malignant ventricular arrhythmias in the absence of cardiac disease or other factors known to precipitate sudden cardiac death. Physicians should be aware of this possible phenomenon in cases of febrile illness associated with syncope.

Aged↗
PubMed1979

[Effect of strophanthin and cytochrome C on myocardial contraction and the incidence of shock and ventricular fibrillation in experimental myocardial infarct].

High ligation of the interventricular artery caused ventricular fibrillation in the first 2--4 minutes in 20% of cats. In the remaining animals myocardial contractility diminished to half its initial value. After that, contractility increased gradually. In cardiosclerosis myocardial contractility reduced by 20--30%. Ligation of the interventricular artery on the background of cardiosclerosis induced cardiogenic shock in half of the animals. Cytochrome C does not reduce the diminution of myocardial contractility after ligation and has a marked antifibrillatory effect. Strophantin does not affect the diminution of contractility of a healthy myocardium but reduces the decrease in contractility of a sclerosed myocardium and also promotes the development of ventricular fibrillation following ligation of the interventricular artery.

Animals↗
PubMed1988

Prevention of ventricular fibrillation with magnesium sulfate.

Mongrel dogs with healed myocardial infarctions were given a 2 min coronary occlusion during an exercise test. The exercise plus ischemia test induced ventricular fibrillation in nine animals. One week later, the test was repeated after pretreatment with magnesium sulfate (100 mg/kg i.v.). Magnesium prevented ventricular fibrillation in seven of the nine animals without adverse side effects. Thus, magnesium may be useful in the management of ventricular fibrillation during ischemia.

Animals↗
PubMed1994

[Comparative study of ischemia-induced and reperfusion-induced ventricular fibrillation in pigs].

To have a better understanding of reperfusion-induced ventricular fibrillation (VF), we studied the relevant morbidity in pigs and compared it with that of the ischemia-induced VF. In 10 hearts of anesthetized chest-open pigs, a total of 127 cycles of various degrees and varied duration of ischemia and reperfusion were completed. VF occurred 13 times (10.2%). Of these, 11 were ischemia-induced VF, while only 2 were reperfusion-induced VF. In two cases of ischemia-induced VF, electric defibrillation failed before the reestablishment of left anterior interventricular branch of coronary artery flow, but after adequate reflowing, all VF turned out to be sinus-rhythm by electric defibrillation. The results suggest that ventricular fibrillation be mainly induced by ischemia but less induced by reperfusion.

Animals↗
PubMed1989

Modulated parasystole as a mechanism of ventricular ectopic activity leading to ventricular fibrillation.

The electrocardiograms of 2 patients with frequent premature ventricular complexes characterized by variable coupling intervals and fusions with sinus activations were analyzed according to the modulated parasystole and reflection hypotheses of Moe et al. In addition, the ectopic activity was associated with couplets, tachycardia and ventricular fibrillation. Departures from the "classic" criteria of parasystole could not be explained satisfactorily if a completely protected (insulated) pacemaker was assumed. In each instance a triphasic response curve could be constructed, suggesting that modulated parasystole was the mechanism common to both patients. Couplets and runs of ventricular tachycardia were ascribed to single and repetitive reflection, respectively, in the presence of supernormal excitability of the ectopic pacemaker, the ventricle or both. In these patients, fibrillation probably resulted from spatial nonuniformity of the ventricular response to the reflected event during a phase of vulnerability. This study suggests that modulated parasystole in the presence of supernormal excitability may lead to very severe arrhythmias and trigger ventricular fibrillation. In the clinical setting, such patients may be misdiagnosed because of atypical features.

Adult↗
PubMed1997

Spatiotemporal complexity of ventricular fibrillation revealed by tissue mass reduction in isolated swine right ventricle. Further evidence for the quasiperiodic route to chaos hypothesis.

We have presented evidence that ventricular fibrillation is deterministic chaos arising from quasiperiodicity. The purpose of this study was to determine whether the transition from chaos (ventricular fibrillation, VF) to periodicity (ventricular tachycardia) through quasiperiodicity could be produced by the progressive reduction of tissue mass. In isolated and perfused swine right ventricular free wall, recording of single cell transmembrane potentials and simultaneous mapping (477 bipolar electrodes, 1.6 mm resolution) were performed. The tissue mass was then progressively reduced by sequential cutting. All isolated tissues fibrillated spontaneously. The critical mass to sustain VF was 19.9 +/- 4.2 g. As tissue mass was decreased, the number of wave fronts decreased, the life-span of reentrant wave fronts increased, and the cycle length, the diastolic interval, and the duration of action potential lengthened. There was a parallel decrease in the dynamical complexity of VF as measured by Kolmogorov entropy and Poincaré plots. A period of quasiperiodicity became more evident before the conversion from VF (chaos) to a more regular arrhythmia (periodicity). In conclusion, a decrease in the number of wave fronts in ventricular fibrillation by tissue mass reduction causes a transition from chaotic to periodic dynamics via the quasiperiodic route.

Action Potentials↗
PubMed1982

[Continuous observation of catecholamine release into the blood of the coronary sinus in experimental myocardial infarct complicated by ventricular fibrillation].

It was established that the content of adrenalin and noradrenalin in the coronary sinus blood increases after occlusion of the coronary artery. In experiments terminating in ventricular fibrillation the concentration of catecholamines was found to be increased more markedly. A temporary correlation was established between an increase in the catecholamine level in the blood of the coronary sinus and the development of ventricular fibrillation. It is assumed that catecholamines are the triggering mechanism in the development of ventricular fibrillation.

Animals↗
PubMed1983

Death in ventricular fibrillation induced by isoproterenol in DOCA-salt pretreated rats preceded by changes in myocardial electrolytes.

Serum and tissue content of sodium, potassium, magnesium and calcium was determined in controls and desoxycorticosterone acetate (DOCA)-salt treated rats to determine whether electrolyte changes preceded the development of isoproterenol-induced death in ventricular fibrillation. Control Sprague Dawley, male rats, were injected subcutaneously (s.c.) with either saline (Group A) or actinomycin D (0.1 mg/kg; Group B) once daily for 4 days. Other rats received 20 mg of DOCA by implantation, drank normal saline and were injected with either saline (Group C) or actinomycin D (Group D) once daily for 4 days. In the first part of the experiment, it was determined that none of 15 rats from Group C died when challenged with isoproterenol (150 micrograms/kg, s.c.) six days later: however, 13 out of 15 rats from Group D died within 29.1 +/- 15.0 minutes (mean +/- S.D.) from isoproterenol injection. Myocardial sodium was elevated (48.8 +/- 3.8 versus 36.3 +/- 1.9) and potassium decreased (60.4 +/- 3.4 versus 70.6 +/- 3.3, meq/kg wet weight, mean +/- S.D.) in rats that had succumbed to isoproterenol. In the second part of the experiment serum and tissues were removed from control and DOCA-saline pretreated rats before they died in ventricular fibrillation, 20 minutes after isoproterenol. DOCA-saline pretreated rats were hypernatremic and hypokalemic and exhibited higher sodium and lower potassium in skeletal muscle than control rats. Isoproterenol elicited hypokalemia in all rats, but it only elevated sodium and decreased potassium content in the myocardium of rats of Group D, that were more prone to die in ventricular fibrillation. It is concluded that myocardial electrolyte changes precede the onset of ventricular fibrillation and may be associated with the development of this dysrhythmia.

Animals↗
PubMed2000

The effects of repeated doses of vasopressin or epinephrine on ventricular fibrillation in a porcine model of prolonged cardiopulmonary resuscitation.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0. 8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 microg/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 +/- 1.5 Hz vs 7. 0 +/- 0.7 Hz (P < 0.001), mean amplitude was 0.65 +/- 0.26 mV vs 0. 21 +/- 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 +/- 9 mm Hg vs 8 +/- 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation.

Animals↗
PubMedDate not supplied

[The structural changes in the lungs in the acute period of a myocardial infarct in the wake of ventricular fibrillation].

Time-related course was studied of structural changes in the lung tissue in acute myocardial infarction having developed in the wake of secondary ventricular fibrillation, using investigational methods common in biology, histochemistry, and electron-microscopy. It has been found out that development in patients with acute myocardial infarction of ventricular fibrillation greatly aggravates the course of the illness inducing origination of profound and even irreversible alternative changes in all constituents of the aerohematic barrier. The above patients developed structural as well as functional pulmonary insufficiency which is at its greatest within 2 to 4 days of the onset of ventricular fibrillation.

Acute Disease↗
PubMed2001

Relationship between serum potassium concentration and risk of recurrent ventricular tachycardia or ventricular fibrillation.

INTRODUCTION: Electrolyte abnormalities are considered a correctable cause of a life-threatening ventricular arrhythmia according to American Heart Association/American College of Cardiology Practice Guidelines, and ventricular tachycardia or ventricular fibrillation in the setting of an electrolyte abnormality is considered a class III indication for defibrillator implantation. However, there are little data to support this recommendation. The purpose of this study was to determine the risk of a recurrent sustained ventricular arrhythmia in patients with a low serum potassium concentration at the time of an initial episode of a sustained ventricular arrhythmia. METHODS AND RESULTS: One hundred sixty-nine consecutive patients who presented with a sustained ventricular arrhythmia and a serum potassium concentration determined on the day of the arrhythmia underwent defibrillator implantation. All patients had structural heart disease and left ventricular ejection fraction of 0.32+/-0.15. On the day of the index arrhythmia, 30% of the patients had a serum potassium concentration <3.5 or >5.0 mEq/L, including 7% who had a serum potassium concentration <3.0 or >6.0 mEq/L. For the entire cohort of patients, freedom from a recurrent sustained ventricular arrhythmia was 18% at 5 years and was not significantly different among patients with a serum potassium concentration <3.5 mEq/L (23%), between 3.5 and 5.0 mEq/L (16%), and >5.0 mEq/L (5%; P = 0.1). CONCLUSION: The results of the present study suggest that patients with structural heart disease and an abnormal serum potassium concentration at the time of an initial episode of sustained ventricular tachycardia or ventricular fibrillation are at high risk for a recurrent ventricular arrhythmia; therefore, implantable defibrillator therapy may be reasonable.

Aged↗
PubMedDate not supplied

[Primary ventricular fibrillation. Clinical features and prognostic significance].

The objective of this study was to evaluate the clinic conditions and the prognosis of patients with primary ventricular fibrillation (PVF) as complication of acute myocardial infarction. We retrospectively analyzed 1,120 patients admitted in Coronary Care Unit within 12 hours of onset of symptoms. PVF (not associated with significative heart failure or shock and occurred within 48 hours of onset of symptoms) occurred in 62 patients (5.53%). The frequency of PVF was highest in patients admitted in the first hours after infarction (p = 0.01) and the inferior localization (p = 0.001). Cigarette smoking was identified as strong independent risk factor for ventricular fibrillation (p = 0.009; relative risk 1.945). A statistically significant excess of pericarditis (p = 0.002), ventricular tachycardia (p = 0.004), atrioventricular block (second-third degree) (p = 0.001) and moderate degree of heart failure (p = 0.003), was found in patients with PVF. The occurrence of PVF was not associated to a significantly higher in hospital mortality rate than that observed in reference group (without ventricular fibrillation) (12.90 vs 14.36%). In the long-term survival at 5 years in patients with PVF, who are discharged alive, was 87.82% vs 80.58% in control group. We conclude: 1. Patients with PVF had more complications rate than among those without it. 2. PVF isn't a marker of increase in hospital death rate. 3. PVF by itself does not indicate an adverse long-term prognosis.

Female↗
PubMed1989

[Long-term (beyond 5 years) prognosis of successfully resuscitated patients with ventricular fibrillation].

An investigation was carried out of 58 patients who had survived ventricular fibrillation during the period 1975-1982 and had been successfully resuscitated in the Cardiologic Clinic of the High Medical Institute in Varna. 12 of the patients were women and 46 were men, mean age 60.8 years (from 43 up to 85 years). 3 of the patients were dropped out of the investigation because of lack of information. 35 patients (63.6%) had died and 20 patients (36.4%) were alive. 4 of the alive patients (20%) had resumed their previous occupation. 3 of the patients (15%) were on old age pension but were engaged in some kind of work. 12 patients (60%) were old age pensioners or on a disablement pension but in good functional class. Only one patient (5%) was in a bad physical condition confined to bed. Ventricular fibrillation has a poor prognosis but if timely and properly treated it could be overcome and the life of the patients could be prolonged. Some of the patients could live a wholesome life for a long period of time (more than 5 years).

Adult↗
PubMed2006

Nonlinear organization of electrocardiogram and optical signals during ventricular fibrillation.

BACKGROUND: Although sympathetic activation may induce ventricular fibrillation (VF), little is known about how the autonomic nervous system influences its nonlinear organization. This study tested the hypothesis that autonomic receptor activation altered the nonlinear organization of VF. METHODS: Isolated rabbit hearts underwent retrograde perfusion with acetylcholine or norepinephrine added to the perfusate. Voltage-sensitive fluorescent images of the ventricular surface were obtained during sustained VF. Concurrent electrocardiogram and optical pixel signals underwent recurrence quantification analysis, which detects and quantifies patterns of repeating data sequences. Recurrence quantification analysis variables signify different aspects of nonlinearity. RESULTS: Recurrence quantification analysis results showed that the electrocardiogram and pixel signals did not exhibit the same pattern of nonlinear organization during VF. Recurrence quantification analysis values were not dramatically altered from baseline by acetylcholine and norepinephrine but instead exhibited considerable variation. CONCLUSION: An alteration in autonomic milieu diminished the nonlinear organization of VF, that is, autonomic receptor activation made VF less likely to behave in a repetitive pattern over time.

Action Potentials↗