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PubMed1996

Induction of ventricular fibrillation predicts sudden death in patients treated with amiodarone because of ventricular tachyarrhythmias after a myocardial infarction.

OBJECTIVE: To examine the value of programmed electrical stimulation of the heart in predicting sudden death in patients receiving amiodarone to treat ventricular tachyarrhythmias after myocardial infarction. DESIGN: Consecutive patients; retrospective study. SETTING: Referral centre for cardiology, academic hospital. PATIENTS: 106 patients with ventricular tachycardia (n = 77) or ventricular fibrillation (n = 29) late after myocardial infarction. INTERVENTIONS: Programmed electrical stimulation was performed while on amiodarone treatment for at least one month. MEASUREMENTS AND MAIN RESULTS: In 80/106 patients either ventricular fibrillation (n = 15) or sustained monomorphic ventricular tachycardia (n = 65) was induced. After a mean follow up of 50 (SD 40) months (1-144), 11 patients died suddenly and two used their implantable cardioverter debfibrillator. By multivariate analysis two predictors for sudden death were found: (1) inducibility of ventricular fibrillation under amiodarone treatment (P << 0.001), and (2) a left ventricular ejection fraction of < 40% (P < 0.05). The survival rate at one, two, three, and five years was 70%, 62%, 62%, and 40% respectively for patients in whom ventricular fibrillation was induced, and 98%, 96%, 94%, 94% for patients with induced sustained monomorphic ventricular tachycardia. Where there was no sustained arrhythmia, five year survival was 100%. CONCLUSIONS: In patients receiving amiodarone because of life threatening ventricular arrhythmias after myocardial infarction, inducibility of ventricular fibrillation, but not of sustained monomorphic ventricular tachycardia, indicates a high risk of sudden death.

Adult↗
PubMed2002

Effect of ventricular fibrillation duration on the defibrillation threshold in humans.

Early during ventricular fibrillation, the defibrillation threshold may be low, as ventricular fibrillation most probably arises from a localized area with only a few wavefronts and the effects of global ischemia, ventricular dilatation, and sympathetic discharge have not yet fully developed. The purpose of this study was to explore the effect of the timing of shock delivery in humans. During implantation of an ICD in 26 patients (24 men, 60 +/- 11 years, 19 coronary artery disease, NYHA 2.2 +/- 0.4, left ventricular ejection fraction 0.42 +/- 0.16), the defibrillation threshold was determined after approximately 10 and 2 seconds of ventricular fibrillation. Ventricular fibrillation was induced by T wave shocks. Mean defibrillation threshold was 9.9 +/- 3.6 J after 10.3 +/- 1.0 seconds. Within 2 seconds, 20 of 26 patients could be successfully defibrillated with < or = 8 J. In these patients, the mean defibrillation threshold was 4.0 +/- 2.1 J after 1.4 +/- 0.3 seconds compared to 9.5 +/- 3.1 J after 10.2 +/- 1.1 seconds (P < 0.001). There were no clinical differences between patients who could be successfully defibrillated within 2 seconds and those patients without successful defibrillation within 2 seconds. In the majority of patients, the defibrillation threshold was significantly lower within the first few cycles of ventricular fibrillation than after 10 seconds of ventricular fibrillation. These results should lead to exploration of earlier shock delivery in implantable devices. This could possibly reduce the incidence of syncope in patients with rapid ventricular tachyarrhythmias and ICDs.

Chi-Square Distribution↗
PubMed1977

Treatment and prevention of primary ventricular fibrillation complicating acute myocardial infarction.

Primary ventricular fibrillation especially occurs during the first hours after acute myocardial infarction and is often not preceded by premonitory ventricular premature beats. In hospital primary ventricular fibrillation can be prevented by an intravenous lidocaine regimen in a rather high dosage. By contrast the effectiveness of intramuscular lidocaine in preventing out-hospital primary ventricular fibrillation is unestablished. If recurrent attacks of primary ventricular fibrillation supervene, intervention with antiarrhythmic therapy and/or cardiac pacing is often unsuccessful. Repeated defibrillation should be carried out under these circumstances. If properly treated primary ventricular fibrillation is associated with a good short and long term prognosis.

Electric Countershock↗
PubMed1994

Double sequential external shocks for refractory ventricular fibrillation.

OBJECTIVES: A technique for terminating refractory ventricular fibrillation is described. BACKGROUND: Refractory ventricular fibrillation can occur in up to 0.1% of electrophysiologic studies. Animal studies have shown that rapid sequential shocks may reduce ventricular fibrillation threshold. METHODS: Five patients of 2,990 consecutive patients in a 3-year period experienced refractory ventricular fibrillation during 5,450 routine electrophysiologic studies. Multiple shocks were delivered by means of a single defibrillator. Double sequential shocks were delivered externally 0.5 to 4.5 s apart by means of two defibrillators with separate pairs of electrodes. RESULTS: In all patients, standard defibrillation was unsuccessful, but all were successfully resuscitated using the double sequential shocks. CONCLUSIONS: This report stresses the importance of an additional defibrillator being readily available during electrophysiologic testing. This technique of rapid, double sequential external shocks may have general applicability, providing a simple and potentially lifesaving approach to refractory ventricular fibrillation.

Electric Countershock↗
PubMed2003

Dynamic nature of electrocardiographic waveform predicts rescue shock outcome in porcine ventricular fibrillation.

STUDY OBJECTIVE: Survival decreases with duration of ventricular fibrillation, and it is possible that failed rescue shocks increase myocardial damage. Structure in the ECG signal during ventricular fibrillation can be quantified by using the scaling exponent, a dimensionless measure that correlates with ventricular fibrillation duration. This study examined whether the scaling exponent could predict rescue shock success and whether unsuccessful rescue shocks altered the structure of the ventricular fibrillation waveform and the responsiveness to subsequent rescue shocks. METHODS: Ventricular fibrillation was electrically induced in 44 anesthetized swine, which were randomly assigned to receive 70-J biphasic rescue shocks at 2, 4, 6, 8, or 10 minutes. If rescue shocks failed, up to 2 subsequent rescue shocks were performed at 2-minute intervals. The scaling exponent was calculated at 1-second intervals from ECG to quantify the organization of the ventricular fibrillation waveform. RESULTS: A total of 92 rescue shocks were delivered, of which 23 successfully converted ventricular fibrillation to an organized rhythm (immediate success). After these 23 rescue shocks, 14 swine sustained organized rhythms for more than 30 seconds (sustained success). Lower scaling exponent values were associated with increased probability of successful rescue shocks. Receiver operating characteristic curves had an area under the curve of 0.86 for immediate rescue shock success and 0.93 for sustained rescue shock success. Failed rescue shocks increased the rate of scaling exponent increase over time but did not appear to affect subsequent rescue shock success when the scaling exponent was taken into account. CONCLUSION: Highly deterministic ventricular fibrillation, reflected by a low scaling exponent, predicted rescue shock success regardless of antecedent failed rescue shocks. In addition, unsuccessful rescue shocks might decrease post-rescue shock ventricular fibrillation waveform organization.

Animals↗
PubMed1994

[The differential characteristics of early ventricular arrhythmias following a myocardial infarct in patients with and without ventricular fibrillation].

OBJECTIVE: To evaluate the characteristics of early ventricular arrhythmias in acute myocardial infarction and their predictive value of ventricular fibrillation. PATIENTS AND METHODS: We retrospectively compared 85 patients who presented ventricular fibrillation with a control group of 187 consecutively acute myocardial infarction patients recorded within the first 12 hours after onset of acute myocardial infarction symptoms. Patients in Killip class III-IV were excluded. RESULTS: In the ventricular fibrillation group we observed a high prevalence of inferior site of infarction (69 vs 56%; p < 0.05), sum of ST in 3 leads (ST-3 leads) with maximal elevation (13 +/- 17 vs 8 +/- 7 mm; p < 0.005), basic heart rate (97 +/- 23 vs 88 +/- 18 bpm; p < 0.01), R-on-T phenomenon (16 vs 2%; p < 0.001). In 22 patients in whom the ventricular fibrillation episode was registered, the basic heart rate preceding the ventricular fibrillation was fast (113 +/- 54 bpm), and the prematurity index (coupling interval/QT) shorter than in the other ventricular arrhythmias (0.9 +/- 0.2 vs 1.2 +/- 0.3 s respectively; p < 0.005). The prematurity index of ventricular arrhythmias in the ventricular fibrillation group was shorter than in the control group (1.2 +/- 0.3 vs 1.5 +/- 0.3 s respectively; p < 0.0001) and the heart rate during runs was faster (172 +/- 54 vs 126 +/- 40 bpm; p < 0.01). The logistic regression analysis showed that R-on-T phenomenon (odds ratio [OR] = 2.8), inferior site of infarct (OR = 3.65), sum of ST-3 leads > 10 mm (OR = 5.82), and basic heart rate > 100 bpm (OR = 2.33) were independent risk factors for ventricular fibrillation. CONCLUSION: Characteristic ventricular arrhythmias were found to precede ventricular fibrillation episodes: R-on-T phenomenon or short prematurity index and fast runs of ventricular tachycardia, with other parameters such a inferior site of infarct, sum of ST-3 leads > 10 mm and basic heart rate > 100 bpm.

Aged↗
PubMed1987

Atrial fibrillation with high degree atrioventricular block masquerading as ventricular fibrillation masquerading as asystole during cardiac arrest.

Ventricular fibrillation (VF) can masquerade as asystole. We report a 54-yr-old male in cardiac arrest who, on surface ECG, appeared to be in VF or asystole. A bedside intracardiac recording using a transmyocardial pacing wire showed the true rhythm to be atrial fibrillation (AF) with high grade atrioventricular block. AF with a high degree block can masquerade as VF, which simultaneously masquerades as asystole, and can be correctly diagnosed by bedside intracardiac monitoring. Patients who have a flat line rhythm which may represent asystole, fine ventricular fibrillation, or atrial fibrillation with a high degree atrioventricular block may warrant a trial of electrical countershock, high-dose atropine, or transthoracic pacing.

Arrhythmias, Cardiac↗
PubMed1986

Potassium channel blockade: A mechanism for suppressing ventricular fibrillation.

The suppression of ventricular fibrillation by antidysrhythmic drugs is well correlated with their ability to block potassium channels in nerve and cardiac membranes. Blockade of potassium channels reduces electrical inhomogeneities in action potential and conduction parameters that lead to ventricular fibrillation. These actions tend to effectively decrease the electrical size of the heart, which suggests a mechanism for antifibrillatory drug action. The receptor sites for antifibrillatory drug action (IK blockade) appear to be on the outside of the cardiac membrane whereas receptors for antiarrhythmic drug action (INa blockade) appear to be on the inside of the cardiac membrane.

4-Aminopyridine↗
PubMed1993

Unfavorable outcome in patients with primary electrical disease who survived an episode of ventricular fibrillation.

BACKGROUND: Prognosis in patients with ventricular tachyarrhythmia without structural heart disease (primary electrical disease) has been described as excellent. However, prognosis may be less favourable in the subgroup surviving an episode of ventricular fibrillation. METHODS AND RESULTS: We prospectively followed 19 consecutive patients (age, 13 to 66 years; mean age, 33 years) who had survived an episode of documented ventricular fibrillation. Structural heart disease, preexcitation, and long QT syndromes were excluded by thorough cardiologic evaluation. All patients underwent 24-hour Holter monitoring, exercise testing, and programmed electrical stimulation according to a standardized protocol. Holter monitoring revealed episodes of ventricular tachyarrhythmia in 5 patients. Exercise testing reproducibly provoked ventricular tachycardia in 2 patients. Baseline programmed electrical stimulation yielded inducibility of rapid ventricular tachyarrhythmia in 10 patients (53%) and noninducibility in 9 (47%). Nine patients were discharged on antiarrhythmic drug therapy. A defibrillator was implanted in 10 patients. During 43-month follow-up (range, 5 to 85 months; median, 41 months), major arrhythmic events recurred in 7 patients (37%). Four of these patients had noninducibility at baseline programmed electrical stimulation. Two patients on antiarrhythmic drugs had recurrent cardiac arrest: one died suddenly and the other was successfully resuscitated from ventricular fibrillation and subsequently underwent defibrillator implantation. In the other 5 patients, termination of (pre)syncopal episodes was associated with defibrillator shocks. Termination of ventricular fibrillation was documented by Holter recording in one of these patients. Specific markers predictive of a recurrent event could not be identified, although 6 of 7 patients with recurrent events had experienced at least one episode of cardiac arrest or (pre)syncope before the index episode. CONCLUSIONS: Patients with primary electrical disease presenting with ventricular fibrillation are at high risk of recurrence of major arrhythmic events during long-term follow-up. Noninducibility at baseline study does not predict an uneventful course. Also, early defibrillator implantation should be considered in these patients.

Adult↗
PubMed1996

Nonlinear dynamics in ventricular fibrillation.

Electrogram recordings of ventricular fibrillation appear complex and possibly chaotic. However, sequences of beat-to-beat intervals obtained from these recordings are generally short, making it difficult to explicitly demonstrate nonlinear dynamics. Motivated by the work of Sugihara on atmospheric dynamics and the Durbin-Watson test for nonlinearity, we introduce a new statistical test that recovers significant dynamical patterns from smoothed lag plots. This test is used to show highly significant nonlinear dynamics in a stable canine model of ventricular fibrillation.

Algorithms↗
PubMed1990

Depletion of myocardial adenosine triphosphate during prolonged untreated ventricular fibrillation: effect on defibrillation success.

We studied left ventricular endomyocardial adenosine triphosphate levels in 13 large mongrel dogs before and during ventricular fibrillation induced cardiac arrest to assess whether myocardial adenosine triphosphate content could predict successful cardiopulmonary resuscitation. Endomyocardial biopsies were performed during sinus rhythm (control), after 15 min of ventricular fibrillation or 10 min of ventricular fibrillation and 5 min of open chest cardiopulmonary resuscitation, after 20 min of ventricular fibrillation and 10 min of open chest cardiopulmonary resuscitation and after 40 min ventricular fibrillation and 15-20 min open chest cardiopulmonary resuscitation. Myocardial adenosine triphosphate was measured utilizing a bioluminescence method adapted for use with endomyocardial biopsies and normalized to protein content. Left ventricular endomyocardial adenosine triphosphate content fell significantly over time from a control level of 8.88 +/- 0.9 micrograms/mg protein to 5.73 +/- 0.5 micrograms/mg protein at 15 min of cardiac arrest, to 3.4 +/- 0.4 micrograms/mg protein after 30 min of cardiac arrest and to 1.98 +/- 0.3 micrograms/mg protein after 60 min of cardiac arrest (P less than 0.001). Adenosine triphosphate levels were significantly different between animals that received 10 min of ventricular fibrillation and successful open chest cardiopulmonary resuscitation and those that received 40 min of ventricular fibrillation and unsuccessful open chest cardiopulmonary resuscitation (4.35 +/- 0.48 vs. 2.11 +/- 0.43 micrograms/mg protein; P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed2002

[A case of ventricular fibrillation during emergency clipping operation for cerebral aneurysm].

A 59 year-old woman with subarachnoid hemorrhage underwent emergency neck clipping of cerebral aneurysm. Her preoperative examination showed atrial fibrillation, pulmonary edema and hypokalemia. Ventricular fibrillation developed immediately after clipping of the aneurysm and recurred 7 times thereafter during the surgery. Hypokalemia was corrected, and hypoxemia and other factors leading to ventricular fibrillation were excluded. RR interval was prolonged prior to ventricular fibrillation. Therefore intravenous temporary cardiac pacemaker was inserted immediately after the end of the surgery. It prevented successfully the prolongation of RR interval as well as ventricular fibrillation. The present case suggests that we should pay attention to the possibility of ventricular fibrillation during emergency radical surgery for ruptured cerebral aneurysm, and that cardiac pacemaker is useful to prevent ventricular fibrillation following prolongation of RR interval.

Anesthesia↗
PubMed1983

Analysis of ambulatory electrocardiograms in 15 patients during spontaneous ventricular fibrillation with special reference to preceding arrhythmic events.

Fifteen patients sustained ventricular fibrillation during ambulatory electrocardiographic recording in a period of 3.5 years over which time 16,500 ambulatory electrocardiograms were analyzed (prevalence = 0.09% or 1/1,100). Eight patients died, and seven survived cardiopulmonary resuscitation. Quantitative analysis of hourly ventricular arrhythmias prior to ventricular fibrillation revealed an increased frequency of premature ventricular beats and ventricular tachycardia, especially in the 2 hours immediately before ventricular fibrillation. Ventricular fibrillation was initiated by ventricular tachycardia in all 15 cases. These runs of ventricular tachycardia were characterized by their unusual length (mean = 560 +/- 536 beats) and their rapid rate (241 +/- 45 beats/min). Although an R on T premature ventricular beat initiated ventricular tachycardia and ventricular fibrillation occasionally, the mean prematurity index of the initiating premature ventricular beat was not early (mean = 1.27 +/- 0.28). QT prolongation was present in only 3 of the 15 patients (mean QTc interval = 0.42 +/- 0.06). Left ventricular dysfunction (mean left ventricular ejection fraction = 34.9 +/- 9.9%) and coronary artery disease were nearly always present. The cardiac medications most frequently associated with these patients at the time of ventricular fibrillation were digitalis and quinidine.

Aged↗