SEARCH · PubMed Health

Results for “VENTRICULAR FIBRILLATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

PubMed1978

Myocardial ultrastructural changes after experimental ventricular fibrillation and anoxic arrest.

A transmural myocardial biopsy method was used to study changed in ultrastructure after induced ventricular fibrillation or anoxic arrest in the canine heart. Interstitial edema, mitochondrial derangement, contraction bands, and swelling of capillary endothelium were more extensive in subendocardial than in subepicardial layer after anoxic arrest. Significant numbers of contraction bands were also seen in the myocardium after induced ventricular fibrillation. These changes appeared to be reversible at least in part in the group with induced ventricular fibrillation but generally not in the anoxic arrest animals. After anoxic arrest, preservation of the endocardial layer was significantly poorer than that of the epicardium; after ventricular fibrillation, there appeared to be no such difference. Myocardial mitochondria and glycogen granules were intact and more numerous after ventricular fibrillation than after anoxic arrest. The lesser damage after ventricular fibrillation than after anoxic arrest suggest that the myocardium may be affected less by the no-reflow phenomenon after normal coronary circulation is restored in ventricular fibrillation.

Animals↗

PubMed1993

Rhythm changes during resuscitation from ventricular fibrillation.

Defibrillation of patients with primary ventricular fibrillation (VF) results in a variety of rhythm changes. We analysed these changes in rhythm in 200 patients, using the American Heart Association's recommendation of two defibrillations prior to drug therapy. Sixty-three (31.5%) patients were immediate survivors with 38 (19%) being discharged from hospital alive. There was no difference between the age of immediate survivors (66.5 years, S.D. = 11.2) and non-survivors (68.3 years, S.D. = 13.7, P = 0.37). Immediate survivors were significantly more likely to be discharged alive from hospital if they were younger (70.0 years, S.D. 8.5 vs. 62.1 years, S.D. 15.8, P = 0.014). Increasing delays to the initiation of basic life support (CPR) and to defibrillation were associated with significantly less likelihood of cardioversion to sinus rhythm (P < 0.005 and P < 0.002, respectively). Those patients who stayed in VF were not more likely to be defibrillated into asystole or electro-mechanical dissociation. Seventeen percent (34) of patients were defibrillated to sinus rhythm after the first defibrillation and 14% (19) after the second, with similar hospital discharge rates (62% and 58%, respectively). Sixty percent (32) of patients in sinus rhythm, after two defibrillations, were discharged alive, compared to only 4% (6) of those patients not in sinus rhythm after two defibrillations. Our data provide new information on rhythm changes during resuscitation and supports the need for the earliest possible initiation of basic life support and defibrillation to improve survival from cardiac arrest due to ventricular fibrillation.

Age Factors↗

PubMed2000

Preventing ventricular fibrillation by flattening cardiac restitution.

Ventricular fibrillation is the leading cause of sudden cardiac death. In fibrillation, fragmented electrical waves meander erratically through the heart muscle, creating disordered and ineffective contraction. Theoretical and computer studies, as well as recent experimental evidence, have suggested that fibrillation is created and sustained by the property of restitution of the cardiac action potential duration (that is, its dependence on the previous diastolic interval). The restitution hypothesis states that steeply sloped restitution curves create unstable wave propagation that results in wave break, the event that is necessary for fibrillation. Here we present experimental evidence supporting this idea. In particular, we identify the action of the drug bretylium as a prototype for the future development of effective restitution-based antifibrillatory agents. We show that bretylium acts in accord with the restitution hypothesis: by flattening restitution curves, it prevents wave break and thus prevents fibrillation. It even converts existing fibrillation, either to a periodic state (ventricular tachycardia, which is much more easily controlled) or to quiescent healthy tissue.

Action Potentials↗

PubMed1992

Direct current application: easy induction of ventricular fibrillation for the determination of the defibrillation threshold in patients with implantable cardioverter defibrillators.

For the determination of the defibrillation threshold, the induction of ventricular fibrillation is mandatory. However, in severely damaged hearts it is sometimes difficult to induce ventricular fibrillation by rapid stimulation or alternating current. Only rapid nonclinical ventricular tachycardias may result, and their cardioversion threshold may be different from the defibrillation threshold. Therefore, it was the purpose of this study to test the potential of direct current (DC) application to rapidly induce ventricular fibrillation in patients with an implanted cardioverter defibrillator. The defibrillation threshold had to be determined in 13 patients (9 with coronary heart disease, 4 with dilative cardiomyopathy, ejection fraction 35%) during and 2 weeks after the implantation of a cardioverter defibrillator. DC was applied 37 times by a commercially available 9-V DC battery via a bipolar catheter for about 3 seconds. Ventricular fibrillation was induced 23 times (62%) and rapid nonclinical ventricular tachycardias were induced six times (16%). In one patient clinical ventricular tachycardia was observed. In seven instances (19%) sinus rhythm remained. In 12 of the 13 patients, ventricular fibrillation could be induced by DC. Thus, the induction of ventricular fibrillation by DC application may serve as an additional tool to induce ventricular fibrillation, determining the defibrillation threshold in implantable cardioverter defibrillator patients.

Cardiac Catheterization↗

PubMed1983

Ventricular fibrillation in hibernators and nonhibernators.

Previous studies have shown that there are differences between hibernators and nonhibernators in the susceptibility to ventricular fibrillation. In an attempt to clarify these differences ventricular fibrillation was induced in isolated hearts of the hibernator, the woodchuck, Marmota monax by cooling, warming, puncture, and by norepinephrine administration. It was shown that the hearts of the winter animals were completely resistant toward the ventricular fibrillation inducing agents, which was not the case for the hearts from summer, active animals. Further, the hearts of another hibernator, the hedgehog, Erinaceus europaeus, and guinea pig, Cavia porcellus, were studied electrophysiologically in anesthetized animals with open chests and with bipolar electrodes attached to the epicardium. During pacing it was shown that the hedgehog had a higher stimulus threshold and a lower maximal following frequency than the guinea pig. The summer hedgehogs showed resistance toward both ventricular premature beats and ventricular fibrillation. Sixty percent of the summer hedgehogs and 100 percent of the winter hedgehogs and guinea pigs developed ventricular fibrillation. The threshold for ventricular fibrillation was highest for summer hedgehogs. The effective refractory period of papillary muscle of summer hedgehogs was shorter than that of guinea pigs. The force frequency relationship of the isolated papillary muscle showed a greater degree of independence in the hedgehog than in the guinea pig. Consequently, the results show that the heart of the hibernator is more arrhythmia resistant than the heart of the nonhibernator, although there are seasonal differences.

Animals↗

PubMed2002

Effects of acute reduction of temperature on ventricular fibrillation activation patterns.

Because of its electrophysiological effects, hypothermia can influence the mechanisms that intervene in the sustaining of ventricular fibrillation. We hypothesized that a rapid and profound reduction of myocardial temperature impedes the maintenance of ventricular fibrillation, leading to termination of the arrhythmia. High-resolution epicardial mapping (series 1; n = 11) and transmural recordings of ventricular activation (series 2; n = 10) were used to analyze ventricular fibrillation modification during rapid myocardial cooling in Langendorff-perfused rabbit hearts. Myocardial cooling was produced by the injection of cold Tyrode into the left ventricle after induction of ventricular fibrillation. Temperature and ventricular fibrillation dominant frequency decay fit an exponential model to arrhythmia termination in all experiments, and both parameters were significantly correlated (r = 0.70, P < 0.0001). Termination of the arrhythmia occurred preferentially in the left ventricle and was associated with a reduction in conduction velocity (-60% in left ventricle and -54% in right ventricle; P < 0.0001) and with activation maps predominantly exhibiting a single wave front, with evidence of wave front extinction. We conclude that a rapid reduction of temperature to <20 degrees C terminates ventricular fibrillation after producing an important depression in myocardial conduction.

Animals↗

PubMed1979

Dibenzepin as an antifibrillatory agent for spontaneously terminating electrically induced ventricular fibrillation.

The effect of dibenzepin, a tricyclic antidepressant drug, on electrically induced ventricular fibrillation was studied in 20 cats and nine dogs. The ventricular fibrillation threshold and the ability of the ventricle to defibrillate spontaneously were determined before and after the administration of dibenzepin, with each animal serving as its own control. The drug raised the ventricular fibrillation threshold in all the animals tested. Before treatment, spontaneous ventricular defibrillation occurred in only 8 of the 20 cats and in none of the dogs. After treatment, all of the cats and eight of the dogs exhibited spontaneous ventricular defibrillation. The study of drugs that have a self-defibrillatory effect may serve to further understanding of the mechanism of ventricular fibrillation and its spontaneous termination.

Animals↗

PubMedDate not supplied

Effect of alpha-adrenergic receptor blockers on the vulnerability of cat heart to ventricular fibrillation.

Recently, alpha-adrenergic receptors have been implicated in the precipitation of arrhythmias associated with myocardial ischemia and reperfusion. The present investigation has been undertaken to study the effect of alpha-adrenoceptor antagonists on electrically induced ventricular fibrillation. The effect of ventricular fibrillation on the alpha-adrenergic receptor population in myocardium and its modification by phentolamine pretreatment has also been investigated. Phentolamine and prazosin raised the ventricular fibrillation threshold significantly. However, yohimbine was protective at high doses only (3 and 5 mg/kg). There was no change in alpha-receptor population and affinity after ventricular fibrillation. Cyclic AMP levels increased in the fibrillating myocardium. Pretreatment with phentolamine did not prevent the decrease in blood flow observed after electrically induced ventricular fibrillation. It is concluded that alpha 1-adrenergic receptor blockade is protective against ventricular fibrillation in cats.

Adrenergic beta-Antagonists↗

PubMed1981

Ischemic ventricular fibrillation: the importance of being spontaneous.

Although the energy level required to defibrillate normal myocardium is low and constant, as determined from studies of induced ventricular fibrillation, little is known of the specific energy requirements in regionally ischemic hearts for spontaneous or induced ventricular fibrillation. In this study the lowest energy threshold for defibrillation was determined in 10 open chest dogs with reversible 10 minute coronary occlusions at various sites for each of 44 events of ventricular fibrillation, using apical and superior vena caval electrodes with a generator providing variable output of 1 to 30 watt seconds. The ischemic mass, quantitated from postmortem angiographic and planimetric data, was 52 +/- 9 percent (mean +/- standard deviation) of the left ventricle in dogs with induced ventricular fibrillation (Group I), 52 +/- 12 percent in dogs with spontaneous ventricular fibrillation after occlusion (Group II) and 54 +/- 9 percent in dogs with spontaneous ventricular fibrillation after reperfusion (Group III). Defibrillation thresholds in watt seconds were 9 +/- 7 in Group I (n = 12), 19 +/- 10 in Group II (n = 13) and 18 +/- 10 in Group II (n = 19). (Group I versus Groups II and III, probability [p] less than 0.025). In nonischemic hearts, the defibrillation threshold was 3 +/- 2 (n = 32) (p less than 0.001 compared with values in Group I, II or III). Thus, despite similar masses of ischemia, twice as much energy was required for defibrillation of spontaneous ventricular fibrillation (whether after occlusion or reperfusion) as for induced ventricular fibrillation, suggesting that these conditions are caused by different metabolic or pathologic derangements. Such differences should be considered in assessing interventions such as drug therapy designed to inhibit the repetitive ventricular response and in design of implantable defibrillators.

Animals↗

PubMed1999

[Idiopathic ventricular fibrillation].

In 1 to 8% of survivors of syncopal ventricular fibrillation, it is impossible to identify a structural cardiac abnormality. Idiopathic ventricular fibrillation, a diagnosis of exclusion, is a term which includes a variety of diseases. This article describes several well defined electro-clinical entities: Brugada's syndrome, torsades de pointes with a short coupling interval, catecholinergic polymorphic ventricular tachycardia and the acquired long QT syndrome. In the majority of these cases, despite the fact that their physiopathology is not fully understood, the management is clear-cut. However, in a large number of patients, the choice between pharmacological treatment and the implantation of an automatic defibrillator remains difficult. Molecular biological studies and strict clinical investigation, standardised with the help of networks, should provide a rational approach to the treatment of idiopathic ventricular fibrillation.

Adult↗

PubMed2001

Antiarrhythmic effects of adenosine on ischemia-induced ventricular fibrillation.

PURPOSE: The antiarrhythmic efficacy of adenosine during states of AV-nodal reentrant tachycardias is well known and clinically established. Adenosine is also able to reduce ventricular arrhythmias when applied before coronary ligation in rats. Hypoxia or ischemia leads to an increased production of adenosine by cardiac myocytes. The purpose of this study was to evaluate if adenosine also has a direct antiarrhythmic effect on ischemia-induced ventricular fibrillation. MATERIALS AND METHODS: In this study, the antiarrhythmic effects of adenosine on ventricular fibrillation during global (low flow) ischemia were evaluated in isolated guinea pig hearts perfused by the method of Langendorff. RESULTS: Adenosine showed a dose-dependent prolongation of the peak to peak interval of the ventricular ECG signal during ventricular fibrillation until ventricular flutter or tachycardia occurred at a concentration of 2 mmol/L. At a concentration of 20 mmol/L, adenosine converted ventricular fibrillation into ventricular tachycardia with intermittent periods of asystole. This conversion of ventricular fibrillation to asystole was antagonised by 200 micromol/L theophylline. CONCLUSION: Adenosine appears to have an antiarrhythmogenic effect both in supraventricular and ventricular rhythm disturbances. During myocardial infarction, where huge amounts of adenosine are present in ischemic regions, asystole may respond to adenosine antagonists.

Adenosine↗

PubMed1990

Ventricular fibrillation during coronary angiography: reduced incidence with nonionic contrast media.

Ventricular fibrillation during coronary angiography with Renografin-76 has been attributed to the high osmolar ionic and calcium binding additive properties. Isovue-370 is a new low osmolar nonionic contrast medium lacking calcium binding additives. The present investigation compared the incidence of contrast media-induced ventricular fibrillation in patients undergoing coronary angiography with Renografin-76 to that with Isovue-370. Group I consisted of 2,000 consecutive patients undergoing coronary angiography with Renografin-76, and group II consisted of 2,000 subsequent consecutive patients in whom Isovue-370 was employed as the contrast medium. There was no significant difference between groups I and II with respect to volume of contrast media used per patient (125 +/- 35 vs. 140 +/- 45 ml), age (63.5 +/- 15 vs. 60 +/- 17 years), sex (74% male vs. 76% male), ejection fraction (55% vs. 55%), valvular heart disease (8% vs. 9%), prior coronary artery bypass graft surgery (5.8% vs. 5%), or extent of coronary artery disease. Contrast media-induced ventricular fibrillation occurred in 20 patients in group I (incidence 1%), whereas eight episodes occurred in group II (incidence 0.4%) (P less than 0.03). Thus the present investigation suggests that the incidence of ventricular fibrillation during coronary angiography can be significantly decreased by using low osmolar nonionic contrast media lacking calcium binding additives.

Angiography↗

PubMed1977

Effects of ventricular fibrillation on coronary blood flow and myocardial metabolism.

Ventricular fibrillation is frequently induced during cardiac surgery to quiet the operative field. The reported effects of fibrillation on the myocardium vary considerably. In an attempt to better define these effects, we subjected 28 dogs to one hour of total normothermic bypass. Myocardial blood flow, lactate, adenosine triphosphate (ATP), oxygen consumption, and left ventricular fibrillation was induced in 5 dogs and continuous electrical fibrillation in 7 dogs. These groups were compared to two respective control groups with beating hearts of 8 animals each. Coronary sinus flow, total coronary blood flow, left ventricular flow, myocardial oxygen consumption, and myocardial tissue lactate increased significantly in the fibrillating hearts. Left ventricular dp/dt decreased with fibrillation, but not significantly. It is concluded that the metabolic demands of ventricular fibrillation exceed the increase in coronary blood flow, when compared to demands of the beating heart, and that decreased left ventricular performance may result.

Adenosine Triphosphate↗

PubMed2001

Pacing during ventricular fibrillation: factors influencing the ability to capture.

INTRODUCTION: Recent studies showed that pacing atrial and ventricular fibrillation (VF) is possible. The studies presented here determined which parameters influence the efficacy of a pacing train to capture fibrillating ventricular myocardium. Electrode type, current strength, order of pacing trains, polarity, and VF morphology preceding the pacing trains were investigated. METHODS AND RESULTS: A 504-electrode recording plaque sutured to the right ventricle of pig hearts was used to record the activations of VF and those resulting from the pacing stimulation. Capture of VF by pacing was determined by observing an animated display of the first temporal derivative of the electrograms. A series of electrodes in a line captured the heart more frequently during VF than did a point electrode. Increasing the current strength to 10 x diastolic pacing threshold increased the incidence of capture, but increasing this strength further did not. The second or third train of 40 stimuli had greater capture rates than did the first train during the same VF episode. Anodal and cathodal unipolar, and bipolar stimulation were equally efficacious in capturing VF. VF activation during the 1-second interval preceding pacing was more organized for pacing trains that captured than those that did not. The highest incidence of capture, 46% to 61% of pacing trains, occurred with a line of electrodes at 10 x diastolic pacing threshold delivered by the second or third train. CONCLUSION: The probability of a pacing train capturing fibrillating myocardium can be influenced by the pacing protocol parameters.

Animals↗

PubMed2000

Prevalence of the Brugada sign in idiopathic ventricular fibrillation and healthy controls.

OBJECTIVE: To determine the prevalence of the Brugada sign (right bundle branch block with ST elevation in V1-V3) in idiopathic ventricular fibrillation and in an age matched healthy population. DESIGN: ECGs from 39 consecutive patients with idiopathic ventricular fibrillation and 592 healthy controls were reviewed. They were classified as definite, questionable, and no Brugada sign (according to predetermined criteria) by four investigators blinded to the subjects' status. RESULTS: Eight patients (21%) with idiopathic ventricular fibrillation but none of the 592 controls had a definite Brugada sign (p < 0.005). Thus the estimated 95% confidence limits for the prevalence of a definite Brugada sign among healthy controls was less than 0.5%. A questionable Brugada sign was seen in two patients with idiopathic ventricular fibrillation (5%) but also in five controls (1%) (p < 0.05). Normal ECGs were found following resuscitation and during long term follow up in 31 patients with idiopathic ventricular fibrillation (79%). Patients with idiopathic ventricular fibrillation and a normal ECG and those with the Brugada syndrome were of similar age and had similar spontaneous and inducible arrhythmias. However, the two groups differed in terms of sex, family history, and the incidence of sleep related ventricular fibrillation. CONCLUSIONS: A definite Brugada sign is a specific marker of arrhythmic risk. However, less than obvious ECG abnormalities have little diagnostic value, as a "questionable" Brugada sign was observed in 1% of healthy controls. In this series of consecutive patients with idiopathic ventricular fibrillation, most had normal ECGs.

Adolescent↗

PubMed1982

A case of arrhythmogenic right ventricular dysplasia with ventricular fibrillation.

A case of repeated attacks of ventricular fibrillation is described. The patient suffered from an arrhythmogenic right ventricular dysplasia (ARVD) documented by right and left ventriculograms and myocardial biopsies obtained during surgical treatment of the arrhythmia. The histological changes were interpreted as being signs of fresh myocardial damage of unknown origin in addition to a replacement of the normal myocardium by adipose and fibrotic tissue. The repeated attacks of ventricular fibrillation in this patient contrast to the arrhythmia spectrum noted in the available literature on ARVD, mostly stable chronic ventricular tachycardias.

Adult↗

PubMed1993

Role of heart mass in the developmental changes of ventricular fibrillation threshold and spontaneous defibrillation in young dogs.

In the course of studying developmental changes of induction and maintenance of ventricular fibrillation in canine pups, we have documented that at about the third week of age, hearts reach a critical point where ventricular fibrillation may become both inducible and sustainable, thus forming the basis for cardiac arrhythmic death. Since age-related variations of cardiac mass may account for these findings, this study was conducted to systematically investigate the role of changing heart mass on the induction and maintenance of ventricular fibrillation in the canine heart, during the early postnatal development. Repetitive determinations of ventricular fibrillation threshold and individual incidence of spontaneous defibrillation were obtained in 87 puppies 1-6 weeks old, from litters of varied body size breeds, studied at weekly intervals. Overall, ventricular fibrillation threshold correlated positively with ventricular weight (VFTmA = 3.30 + 1.27 Vwtg, r = 0.71). However the slopes were steeper and correlations were stronger for the first, second and sixth week and nonsignificant in the fourth and fifth weeks. The ventricular fibrillation to ventricular weight ratio also varied with age (P < 0.01). Spontaneous defibrillation occurred at least once in 68 of the puppies (78%). In general, spontaneous defibrillation was more likely to occur in hearts weighing less than 9 grams (P < 0.01), but the overall correlation of the decreasing defibrillation incidence to increasing weight was weak (SDF % = 48.6-0.90 Vwtg, r = 0.106). Spontaneous defibrillation was not observed at any age or weight in two litters, totaling 9 puppies.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1994

Effect of bretylium tosylate on ventricular fibrillation threshold during hypothermia in dogs.

How bretylium tosylate affected the ventricular fibrillation threshold, electrophysiological parameters, and plasma catecholamine levels during hypothermia in dogs was studied. Threshold for ventricular fibrillation was determined by programmed electrical stimulation using a stimulation protocol that involved applying a maximum of five extrastimuli at body temperatures 37, 34, 31, 28, and 25 degrees C, and at the same temperatures during rewarming. Electrocardiogram, epicardial monophasic action potentials (MAP), and electrograms were recorded, and ventricular effective refractory period (VERP) was determined at each of the above temperatures. In one group (n = 7), a bolus dosage of bretylium tosylate (BT), 6 mg/kg body wt, was administered at 25 degrees C before rewarming. Another group (n = 4) was exposed to cooling and rewarming without addition of BT. Cooling to 25 degrees C reduced ventricular fibrillation threshold linearly, reduced heart rate, increased VERP and MAP, and slowed myocardial conduction velocity in both groups. There was no overall increase in plasma catecholamine levels during cooling. Addition of BT at 25 degrees C increased ventricular fibrillation threshold during rewarming compared with cooling. Addition of BT at 25 degrees C increased VERP by +/- 32 milliseconds and the corrected JT time by 0.06 +/- 0.02 seconds. VERP and JTc increased during rewarming with BT compared with cooling with no drug. BT had no effect on conduction velocity, and plasma catecholamine levels were not reduced. The antiarrhythmic effect of BT during hypothermia was attributed to an increased wavelength of refractoriness by its increase in the refractory period. This increased wavelength of refractoriness may prevent excitable gaps or increase circuit pathway in the setting of reentry arrhythmias.

Action Potentials↗