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PubMed1995

[Ventricular fibrillation and defibrillation; electrophysiological bases and clinical applications].

During sinus rhythm, the successive responses to the application of electrical stimuli of increasing intensity during the vulnerable period are cardiac stimulations followed by repetitive ventricular responses and then ventricular fibrillation. An impulse of even greater intensity is not followed by ventricular fibrillation (shock at the upper limit of vulnerability) suggesting that defibrillatory shock is effective only when it does not reinduce fibrillation. Two other hypotheses are also proposed in fibrillation, that of critical mass and that of extension of the refractory periods, in particular after biphasic shocks. Clinically, the measurement of the threshold of defibrillation is difficult as it is a random process which does not obey the all or nothing principle. Ideally, a graph of efficacy versus energy should be constructed but this is only possible under experimental conditions. The effects of different antiarrhythmic drugs have been studied in this manner; in general, the sodium channel blockers improve the energies of defibrillation.

Animals↗

PubMed2000

Ventricular fibrillation in a patient with prominent J (Osborn) waves and ST segment elevation in the inferior electrocardiographic leads: a Brugada syndrome variant?

Recurrent ventricular fibrillation was observed in a 29-year-old Vietnamese man who did not exhibit structural heart disease. The patient's ECG showed prominent J (Osborn) waves and ST segment elevation in the inferior leads that were not associated with hypothermia, serum electrolyte disturbance, or myocardial ischemia. Rate-dependent change in the amplitude of J waves and ST segment elevation also were observed. An implantable cardioverter defibrillator (ICD) was implanted. Adjunctive treatment with amiodarone reduced J wave amplitude, preventing ventricular fibrillation and ICD shocks. Prominent J waves and ST segment elevation in the inferior leads may serve as an important diagnostic sign to detect high-risk individuals with a history of unexplained syncope. ICD implantation plus amiodarone is the treatment of choice.

Adult↗

PubMed2002

Effects of amiodarone on wave front dynamics during ventricular fibrillation in isolated swine right ventricle.

The effects of acute amiodarone infusion on dynamics of ventricular fibrillation (VF) are unclear. Six isolated swine right ventricles (RVs) were studied in vitro. Activation patterns during VF were mapped optically, whereas action potentials were recorded with a glass microelectrode. At baseline, VF was associated with frequent spontaneous wave breaks. Amiodarone (2.5 microg/ml) reduced spontaneous wave breaks and increased the cycle length (CL) of VF from 83.3 +/- 17.8 ms at baseline to 118.4 +/- 25.8 ms during infusion (P < 0.05). Amiodarone increased the reentrant wave front CL (114.4 +/- 15.5 vs. 78.2 +/- 19.0 ms, P < 0.05) and central core area (4.1 +/- 3.8 vs. 0.9 +/- 0.3 mm2, P < 0.05). Within 30 min of infusion, VF terminated (n = 1), converted to ventricular tachycardia (VT) (n = 1) or continued at a slower rate (n = 4). Amiodarone flattened the APD restitution curves. We conclude that amiodarone reduced spontaneous wave breaks. It might terminate VF or convert VF to VT. These effects were associated with the flattening of APD restitution slope and increased core size of reentrant wave fronts.

Action Potentials↗

PubMed1981

Comparison of bretylium tosylate and lidocaine in management of out of hospital ventricular fibrillation: a randomized clinical trial.

Bretylium tosylate was compared with lidocaine hydrochloride as initial drug therapy in 146 victims of out of hospital ventricular fibrillation in a randomized blinded trial. An organized rhythm was achieved in 89 and 93 percent and a stable perfusing rhythm in 58 and 60 percent of the patients who received bretylium and lidocaine, respectively. After initiation of advanced life support, an organized rhythm was first established after an average of 10.4 minutes and 10.6 minutes in the two respective groups, requiring an average of 2.8 defibrillatory shocks in those who received bretylium and 2.4 in the lidocaine-treated patients. Comparable numbers of patients were discharged from the hospital: 34 percent of those given bretylium and 26 percent of the patients whose initial therapy was lidocaine. No instance of chemical defibrillation was observed with either drug. In this study, bretylium afforded neither significant advantage nor disadvantage compared with lidocaine in the initial management of ventricular fibrillation.

Bretylium Compounds↗

PubMed1990

Nimodipine after resuscitation from out-of-hospital ventricular fibrillation. A placebo-controlled, double-blind, randomized trial.

One hundred fifty-five consecutive patients resuscitated after out-of-hospital ventricular fibrillation by a physician-manned advanced life support unit were randomly assigned to receive nimodipine or placebo at a dosage of 10 micrograms/kg as an intravenous injection immediately after restoration of spontaneous circulation, followed by an infusion of 0.5 micrograms/kg per minute for 24 hours. No significant difference was found in the 1-year survival rate of nimodipine-treated (30 [40%] of 75 patients) and placebo-treated patients (29 [36%] of 80 patients). Recurrent ventricular fibrillation during the treatment occurred in one patient in the nimodipine group compared with 12 patients in the placebo group. In a post hoc analysis of patients with very long delays in advanced life support (more than 10 minutes), the 1-year survival rate was higher with nimodipine (eight [47%] of 17 patients) than with placebo (two [8%] of 26 patients). Nimodipine may be of benefit in patients with delayed resuscitation.

Aged↗

PubMed1979

Ventricular tachycardia and ventricular fibrillation in a young population.

In this study, we describe the findings in 18 young patients (age range 4 days to 24 years, mean 16.6 years) who had ventricular tachycardia and/or ventricular fibrillation and were followed for 4--70 months (mean 22.4 months). Patients had a variety of problems associated with their arrhythmia, including mitral valve prolapse, cardiomyopathy, myocarditis, prolonged QT syndrome and hypokalemia. Six patients had no clinically recognizable cardiac abnormality. The ventricular tachycardia showed a left bundle branch block contour in 10 of 17 patients, right bundle branch block in four, was multiform in two and had an indeterminate contour in one. Sustained ventricular tachycardia was initiated and terminated reproducibly by atrial and ventricular stimulation in three of seven patients who did not have spontaneous episodes of ventricular tachycardia during the electrophysiologic study. In one other patient, short bursts of ventricular tachycardia were induced. Patients who had ventricular fibrillation, those who died, and those who are still symptomatic with poorly controlled ventricular arrhythmias had significant heart disease. In one patient, a ventricular tachyarrhythmia that had required more than 100 electrical cardioversions spontaneously disappeared after requiring 1 year of antiarrhythmic therapy.

Adolescent↗

PubMed2001

Patterns of wave break during ventricular fibrillation in isolated swine right ventricle.

Several different patterns of wave break have been described by mapping of the tissue surface during fibrillation. However, it is not clear whether these surface patterns are caused by multiple distinct mechanisms or by a single mechanism. To determine the mechanism by which wave breaks are generated during ventricular fibrillation, we conducted optical mapping studies and single cell transmembrane potential recording in six isolated swine right ventricles (RV). Among 763 episodes of wave break (0.75 times x s(-1) x cm(-2)), optical maps showed three patterns: 80% due to a wave front encountering the refractory wave back of another wave, 11.5% due to wave fronts passing perpendicular to each other, and 8.5% due to a new (target) wave arising just beyond the refractory tail of a previous wave. Computer simulations of scroll waves in three-dimensional tissue showed that these surface patterns could be attributed to two fundamental mechanisms: head-tail interactions and filament break. We conclude that during sustained ventricular fibrillation in swine RV, surface patterns of wave break are produced by two fundamental mechanisms: head-tail interaction between waves and filament break.

Action Potentials↗

PubMed1984

Primary ventricular fibrillation complicating acute myocardial infarction: an assessment of predictability and prognosis.

In order to identify patients with a high risk of developing primary ventricular fibrillation (PVF) following acute myocardial infarction (AMI) and to examine the prognostic significance of this arrhythmia, 46 patients who developed PVF were compared to a group of 80 patients who had AMI without PVF. A computerized, multivariate discriminant analysis identified several significant correlates of PVF. Higher rates of hypokalemia, complete left bundle branch block, 3rd-degree AV block and a lower frequency of diabetes were found in the PVF group. No difference was found with respect to the frequency of warning arrhythmias. A discriminant function constructed on the basis of the significant variables had a 4.3% false-negative rate in predicting PVF. Recurrent ventricular fibrillation occurred in nine patients, four of whom died. In-hospital mortality was significantly higher in the PVF than in the control group. As PVF is associated, in part, with treatable derangements and increased mortality, every endeavor should be made to prevent its occurrence.

Aged↗

PubMedDate not supplied

Early out-of-hospital lidocaine administration decreases the incidence of primary ventricular fibrillation in acute myocardial infarction.

This study was designed to assess the effectiveness of early prehospital intravenous administration of lidocaine in preventing primary ventricular fibrillation (PVF) in patients with suspected acute myocardial infarction (AMI). Sixty patients with suspected AMI, seen by the Mobile Coronary Care Unit (MCCU) of Florence, were randomly allocated at home to treatment with lidocaine (bolus i.v. of 1 mg/kg, followed by an infusion of 4 mg/min) or placebo (infusion of saline at a rate of 1 mL/min), respectively. The lidocaine group (27 patients) and the control group (33 patients) were not significantly different in age, clinical condition, or time of randomization. The diagnosis of AMI was confirmed in all 60 patients during the hospital stay. Ventricular fibrillation (VF) occurred in 5 patients in the control group in comparison to none in the lidocaine group (P < 0.05). Three patients experienced VF at home and were successfully resuscitated by an MCCU cardiologist. In another two patients, VF occurred during the first 4 hours after onset of symptoms. No major side effects were observed after the infusion of lidocaine. Our findings support the effectiveness of the prophylactic administration of lidocaine in preventing PVF in the prehospital phase of AMI and suggest that the drug can be safely administered in this setting by prehospital personnel.

Aged↗

PubMed1999

The influence of ventricular fibrillation duration on defibrillation efficacy using biphasic waveforms in humans.

OBJECTIVES: The purpose of this study was to prospectively investigate the influence of ventricular fibrillation (VF) durations of 5, 10 and 20 s on the defibrillation threshold (DFT) during implantable cardioverter-defibrillator (ICD) implantation. BACKGROUND: Although the DFT using monophasic waveforms has been shown to increase with VF duration in humans, the effect of VF duration on defibrillation efficacy using biphasic waveforms in humans is not known. METHODS: Thirty patients undergoing primary ICD implantation or pulse generator replacement were randomly assigned to have the DFT determined using biphasic shocks at two durations of VF each (5 and 10 s, 10 and 20 s or 5 and 20 s). RESULTS: There was no statistically significant difference in the mean DFT comparing VF durations of 5 s (9.5+/-6.0 J) and 10 s (10.8+/-7.0 J) (p=0.4). The mean DFT significantly increased from 10.9+/-6.1 J at 10 s of VF to 12.6+/-5.6 J (p=0.03) at 20 s of VF, and from 7.0+/-3.5 J at 5 s of VF to 10.5+/-6.3 J (p=0.04) at 20 s of VF. An increase in the DFT was observed in 14 patients as VF duration increased. There were no clinical characteristics that differentiated patients with and without an increase in the DFT. CONCLUSIONS: Defibrillation efficacy decreases with increasing VF duration using biphasic waveforms in humans. Ventricular fibrillation durations greater than 10 s may negatively affect the effectiveness of ICD therapy.

Aged↗

PubMed2004

Ventricular fibrillation: new insights into mechanisms.

Device therapy with implantable cardioverter-defibrillators is currently the only proven effective therapy against sudden cardiac death due to ventricular fibrillation. However, the expanded clinical indications for device therapy come at a staggering cost to an already overburdened health care system. Given these statistics, it is both highly desirable and economically imperative to develop alternative therapies. New insights into the mechanisms of ventricular fibrillation, particularly the role of dynamic factors causing wave instability, are providing a promising avenue for developing novel therapies to prevent sudden cardiac death.

Action Potentials↗

PubMed1992

Development of cardiac innervation, ventricular fibrillation, and sudden infant death syndrome.

The effects of bilateral vagotomy and of right, left, and bilateral stellectomy on sinus node and on ventricular fibrillation threshold (VFT) were assessed in three groups of puppies (1, 3, and 5 wk old) and one group of adult dogs. Heart rate was increased by vagotomy and reduced by right stellectomy in all groups. After vagotomy, VFT did not change in the first week, while it decreased in the third week (-21%, P < 0.0001), in the fifth week (-20%, P < 0.001) and in the adults dogs (-18%, P < 0.005). VFT was not modified by right stellectomy in the first week and in the fifth week (0%, NS), while it decreased in the third week (-28%, P < 0.05) and in the adults (-32%, P < 0.001). Left stellectomy, performed after right stellectomy, increased VFT in the third week (+52%, P < 0.05), in the fifth week (+62%, P < 0.001), and in the adults (+45%, P < 0.01). Thus removal of either vagal or right cardiac sympathetic activity increases susceptibility to ventricular fibrillation already during the first weeks of life. By contrast, removal of left sympathetic nerves increases cardiac electrical stability. These findings are consistent with the hypothesis that a developmental abnormality in cardiac innervation may play a role in the genesis of some cases of sudden infant death syndrome.

Aging↗

PubMed1999

Ventricular fibrillation: an extreme presentation of primary hyperaldosteronism.

Patients with primary aldosteronism often present with hypokalemia and hypertension. Primary aldosteronism presenting as sudden death due to ventricular fibrillation is described in an otherwise healthy 37-year-old woman. After successful direct current cardioversion, serum potassium was 1.4 mmol/L. Investigations revealed a suppressed renin level, elevated serum aldosterone and a right adrenal nodule found on imaging. Ventricular fibrillation has not previously been described as a presention of a biochemically and surgically proven aldosterone-producing adenoma. This case highlights the importance of early detection and proper diagnosis of secondary hypertension before serious sequelae occur.

Adrenal Cortex Neoplasms↗

PubMed1991

Effects of ethinyl estradiol on isoproterenol-induced death in ventricular fibrillation in DOCA-salt pretreated male and female rats.

To assess the effects of ethinyl estradiol on the incidence of death in ventricular fibrillation induced by isoproterenol in DOCA-salt pretreated rats we implanted male and female rats simultaneously with a 20 mg DOCA pellet and pellets containing either ethinyl estradiol or vehicle (wax). Rats drank saline after implantation. After 6 days rats were challenged with a single, sc dose of 150 micrograms of isoproterenol. The average daily dose of estradiol per rat was estimated on the basis of the quantity of pellet lost during 6 days. In male rats the average daily dose of 61.2 +/- 20.2 micrograms/rat of ethinyl estradiol decreased the incidence of mortality by 80%, from 73.3% (11/15) in vehicle treated to 13.3% (2/15) in estradiol treated rats. Death occurred within 19.2 +/- 8.0 minutes from the injection of isoproterenol and was due to ventricular fibrillation. Serum levels of magnesium and potassium were comparable in the two groups both before and after isoproterenol. Isoproterenol induced death in 9 of 11 DOCA-salt pretreated, ovariectomized rats within 22.3 +/- 9.8 minutes. Only 3 of 11 DOCA-salt ovariectomized rats receiving the average daily dose of 28.4 +/- 12.1 micrograms/rat of ethinyl estradiol died. None of 10 ovariectomized untreated rats died from isoproterenol challenge. Serum levels of magnesium and potassium were comparable in the estradiol and vehicle treated groups. The average daily dose of 2.8 +/- 0.42 micrograms/rat of ethinyl estradiol elicited uterine growth but did not influence the incidence of mortality, since 9 out of 16 and 10 out of 16 rats died following isoproterenol in vehicle and estradiol treated DOCA-salt ovariectomized rats. We conclude that only pharmacological doses of estradiol exert protective effects against DOCA-salt induced myocardial sensitization to isoproterenol and that this protection is not associated with relevant changes in serum potassium or magnesium.

Animals↗

PubMed1997

Asphyxiation versus ventricular fibrillation cardiac arrest in dogs. Differences in cerebral resuscitation effects--a preliminary study.

UNLABELLED: We explored the hypothesis that brain damage after cardiac arrest caused by ventricular fibrillation (VF) needs different therapies than that after asphyxiation, which has been studied less thoroughly. In 67 healthy mongrel dogs of both sexes cardiac arrest (at normothermia) by ventricular fibrillation (no blood flow lasting 10 min) or asphyxiation (no blood flow lasting 7 min) was reversed by normothermic external cardiopulmonary resuscitation, followed by intermittent positive-pressure ventilation for 20 h, and intensive care to 96 h. To ameliorate ischemic brain damage, the calcium entry blocker lidoflazine or a solution of free radical scavengers (mannitol and L-methionine in dextran 40) plus magnesium sulphate, was given intravenously immediately upon restoration of spontaneous circulation. Outcome was evaluated as functional deficit, brain creatine kinase (CK) leakage into the cerebrospinal fluid (CSF) and brain morphologic changes. Lidoflazine seemed to improve cerebral outcome after VF but not after asphyxiation. Free radical scavengers plus magnesium sulphate seemed to improve cerebral outcome after asphyxiation, but not after VF. After VF, scattered ischemic neuronal changes in multiple brain regions dominated, and total brain histopathologic damage scores correlated with final neurologic deficit scores at 96 h (r = 0.66) and with peak CK levels in CSF (r = 0.81). After asphyxiation, in addition to the same ischemic neuronal changes, microinfarcts occurred, and there was no correlation between total brain histopathologic damage scores and neurologic deficit scores or CK levels in CSF. CONCLUSIONS: Different mechanisms of cardiac arrest, which cause different morphologic patterns of brain damage, may need different cerebral resuscitation treatments.

Animals↗

PubMed1984

Fluctuations in T-wave morphology and susceptibility to ventricular fibrillation.

Susceptibility of the ventricles to fibrillation has been related to the degree of spatial inhomogeneity in the repolarization process. We studied the pattern of beat-to-beat fluctuations in ventricular repolarization processes in order to determine whether a relationship also exists between the temporal variability of ventricular repolarization and susceptibility to ventricular fibrillation. We used the morphology of the T-wave recorded in surface and epicardial leads as a measure of the ventricular repolarization process. The Ventricular Fibrillation Threshold (VFT) was used as the standard measure of cardiac susceptibility to fibrillation. In dog experiments, T-wave morphologic indices were computed on 1,024 sequential beats. Histogram, autocorrelation and power spectrum analyses were performed on the sequence of T-wave morphologic indices. A series of 27 experiments were performed on 20 dogs in which VFT was reduced by several different interventions--hypothermia, tachycardia and coronary artery ligation. For all three interventions we observed the same characteristic change in the pattern of T-wave morphology fluctuations. In particular, we found that as the VFT was reduced, a pattern of T-wave alternans developed. This pattern was generally not detectable by visual inspection of the ECG. It was, on the other hand, easily quantified in terms of a T-wave alternans index (TWAI) which we computed from the power spectrum of the T-wave fluctuations. In 26 of the 27 experiments, measured VFT decreased (p less than .001); in 20 of these experiments the TWAI computed from the surface ECG increased (decreased) when VFT decreased (increased) (p less than .01). In 17 experiments epicardial electrograms were recorded. In 16 of these experiments VFT decreased (p less than .001). In 16 of these 17 experiments TWAI computed from the epicardial ECG increased (decreased) when the VFT decreased (increased) (p less than .001). We conclude that statistical analysis of fluctuations in ECG complex morphology may provide a sensitive probe of ventricular vulnerability to fibrillation.

Animals↗

PubMed2003

Ventricular fibrillation during electrical cardioversion of pre-excited atrial fibrillation.

The Wolff-Parkinson-White syndrome can rarely present with pre-excited atrial fibrillation. In this condition the short refractory period of the accessory pathway can lead to rapid atrioventricular conduction. There is then a danger that at high heart rates the irregular broad complex tachycardia that results can deteriorate into ventricular fibrillation. The initial management of patients presenting in pre-excited atrial fibrillation requires cardioversion to sinus rhythm. This can be performed by DC cardioversion or pharmacological means. This paper describes the case of a patient presenting in pre-excited atrial fibrillation where electrical DC cardioversion lead to transient iatrogenic ventricular fibrillation.

Adult↗

PubMed2000

High dispersion of ventricular repolarization after an implantable defibrillator shock predicts induction of ventricular fibrillation as well as unsuccessful defibrillation.

OBJECTIVES: To test the hypothesis that post-shock dispersion of repolarization (PSDR) is higher in T wave shocks that induce ventricular fibrillation (VF) than in those that do not, as well as in implantable cardioverter defibrillator (ICD) defibrillation shocks which fail to terminate VF when compared with those that are successful. BACKGROUND: Ventricular fibrillation has been linked to the presence of dispersion of repolarization, which facilitates reentry. Most of the studies have been done in animals, and the mechanism underlying the generation and termination of VF in humans is speculative and remains to be determined. METHODS: Monophasic action potentials (MAPs) were recorded simultaneously from the right ventricular outflow tract (RVOT) and the right ventricular apex (RVA) in 27 patients who underwent implantation and testing of an ICD. T wave shocks were used to induce VF while the termination was attempted using internal defibrillator shocks. The post-shock repolarization time (PSRT) was measured in both the RVA and RVOT MAPs, and the difference between the two recordings was defined as the PSDR. The averages of PSDR were compared between the successful and unsuccessful inductions and terminations of VF. RESULTS: T wave shocks that induced VF generated a greater PSDR (93.4 +/- 85.1 ms) than the unsuccessful ones (45.1 +/- 55.9 ms, p < 0.001). On the other hand, shocks that failed to terminate VF were associated with a greater PSDR (59.9 +/- 41.2 ms) than shocks that terminated VF (21.1 +/- 20.1 ms), p < 0.001. CONCLUSIONS: A high PSDR following a T wave shock is associated with induction of VF; while following a defibrillating shock, it is associated with its failure and the continuation of VF. Conversely, a low PSDR is associated with failure of a T wave shock to induce VF and successful termination of VF by a defibrillating shock.

Action Potentials↗