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At least 55 records · Page 3Linked to original sources
PubMed1993

Physiologic measurement of the ventricular fibrillation ECG signal: estimating the duration of ventricular fibrillation.

Estimating the duration of ventricular fibrillation may help determine the best initial therapy and provide estimates of the most appropriate dose of epinephrine to administer during cardiac arrest and resuscitation. In addition, estimating this time can provide a more sound methodologic approach to stratifying patients in the analysis of cardiac arrest studies. In an initial series of studies in swine, we attempted to determine whether changes in the frequency or amplitude (power) of the ventricular fibrillation ECG signal during cardiac arrest could be used to estimate this time. These studies characterized the dynamics of both the total power and the frequency distribution of the power in the ECG over time during ventricular fibrillation in swine. Our purpose was to determine whether sufficient information existed in either parameter to estimate the duration of ventricular fibrillation. The median frequency of the power spectrum was used to track power distribution. Both parameters followed a dynamic and repeatable pattern. A mathematical model of median frequency was developed and used with data obtained from additional swine to estimate the duration of ventricular fibrillation. The model estimated the duration of ventricular fibrillation to within +/- 1.3 minutes of the actual duration from one to ten minutes after the onset of ventricular fibrillation. We recently characterized the time course of the median frequency during ventricular fibrillation in human beings. The median frequency was extracted from each four-second segment of the ventricular fibrillation ECG recordings and plotted versus time from the onset of cardiac arrest. The median frequency in human beings followed a repeatable time course during ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Limited value of programmed electrical stimulation from multiple right ventricular pacing sites in clinically sustained ventricular fibrillation or ventricular tachycardia associated with coronary artery disease.

One-hundred and fifty patients with coronary artery disease and a documented history of sustained ventricular tachyarrhythmias were studied to determine if programmed electrical stimulation (PES) from a second right ventricular (RV) pacing site optimizes the induction of such sustained arrhythmias. The first PES test was performed from 2 RV pacing sites (apex and outflow tract or septum) using the apex first in each patient. All patients underwent a second PES within 6 to 24 hours of the first; both studies used up to 4 ventricular extrastimuli, in the absence of antiarrhythmic treatment. The second PES was performed from a single RV apical site using a pacing catheter retained from the first study. During the first day's study, 74 patients (49%) had sustained ventricular tachycardia induced from the RV apex. Only 11 of the remaining 76 patients (7% of the total group) were inducible exclusively from a second RV pacing location during the first day's testing. Seven of these 11 patients, as well as 15 additional patients who did not have ventricular tachycardia induced from either site on the first day's study, were inducible from the RV apex during the second drug-free study. Among patients with sustained ventricular tachyarrhythmias, limiting PES to a single RV site, with the option of performing a second study in those who are initially noninducible is more effective in inducing sustained ventricular tachyarrhythmias than is PES performed from 2 RV pacing sites.

Adult↗
PubMed2005

Malignant entity of idiopathic ventricular fibrillation and polymorphic ventricular tachycardia initiated by premature extrasystoles originating from the right ventricular outflow tract.

OBJECTIVES: The aim of this study was to assess the clinical characteristics and the efficacy of radiofrequency catheter ablation (RFCA) for idiopathic ventricular fibrillation (VF) and/or polymorphic ventricular tachycardia initiated by ventricular extrasystoles originating from the right ventricular outflow tract (RVOT). BACKGROUND: Ventricular fibrillation and/or polymorphic ventricular tachycardia are occasionally initiated by ventricular extrasystoles originating from the RVOT in patients without structural heart disease. METHODS: Among 101 patients without structural heart disease in whom RFCA was conducted for idiopathic ventricular tachyarrhythmias arising from the RVOT, we examined the clinical characteristics and the efficacy of RFCA in 16 patients with spontaneous VF and/or polymorphic ventricular tachycardia initiated by the ventricular extrasystoles originating from the RVOT. RESULTS: Among 16 patients, spontaneous episodes of VF were documented in 5 patients, and 11 patients had prior episodes of syncope. Holter recordings showed frequent isolated ventricular extrasystoles with the same morphology as that of initiating ventricular extrasystoles, and non-sustained polymorphic ventricular tachycardia with short cycle length (mean of 245 +/- 28 ms) in all 16 patients. Radiofrequency catheter ablation by targeting the initiating ventricular extrasystoles eliminated episodes of syncope, VF, and cardiac arrest in all patients during follow-up periods of 54 +/- 39 months. CONCLUSIONS: Our data suggest that the malignant entity of idiopathic VF and/or polymorphic ventricular tachycardia was occasionally present in patients with idiopathic ventricular arrhythmias arising from the RVOT. Radiofrequency catheter ablation was effective as a treatment option for this entity.

Adult↗
PubMed2006

Vasopressin improves outcome in out-of-hospital cardiopulmonary resuscitation of ventricular fibrillation and pulseless ventricular tachycardia: a observational cohort study.

INTRODUCTION: An increasing body of evidence from laboratory and clinical studies suggests that vasopressin may represent a promising alternative vasopressor for use during cardiac arrest and resuscitation. Current guidelines for cardiopulmonary resuscitation recommend the use of adrenaline (epinephrine), with vasopressin considered only as a secondary option because of limited clinical data. METHOD: The present study was conducted in a prehospital setting and included patients with ventricular fibrillation or pulseless ventricular tachycardia undergoing one of three treatments: group I patients received only adrenaline 1 mg every 3 minutes; group II patients received one intravenous dose of arginine vasopressin (40 IU) after three doses of 1 mg epinephrine; and patients in group III received vasopressin 40 IU as first-line therapy. The cause of cardiac arrest (myocardial infarction or other cause) was established for each patient in hospital. RESULTS: A total of 109 patients who suffered nontraumatic cardiac arrest were included in the study. The rates of restoration of spontaneous circulation and subsequent hospital admission were higher in vasopressin-treated groups (23/53 [45%] in group I, 19/31 [61%] in group II and 17/27 [63%] in group III). There were also higher 24-hour survival rates among vasopressin-treated patients (P < 0.05), and more vasopressin-treated patients were discharged from hospital (10/51 [20%] in group I, 8/31 [26%] in group II and 7/27 [26%] group III; P = 0.21). Especially in the subgroup of patients with myocardial infarction as the underlying cause of cardiac arrest, the hospital discharge rate was significantly higher in vasopressin-treated patients (P < 0.05). Among patients who were discharged from hospital, we found no significant differences in neurological status between groups. CONCLUSION: The greater 24-hour survival rate in vasopressin-treated patients suggests that consideration of combined vasopressin and adrenaline is warranted for the treatment of refractory ventricular fibrillation or pulseless ventricular tachycardia. This is especially the case for those patients with myocardial infarction, for whom vasopressin treatment is also associated with a higher hospital discharge rate.

Adult↗
PubMedDate not supplied

Detection of ventricular fibrillation with a ventricular monopolar catheter electrode.

This report describes the use of right ventricular impedance (RVZ) sensing with a monopolar electrode to identify the cessation of pumping with the onset of ventricular fibrillation. RVZ, ECG (lead II), and femoral artery pressure were monitored in seven anesthetized dogs. An impedance recorder (10-kHz, 100-microA peak-to-peak current) was used to measure RVZ between a monopolar, catheter-mounted electrode placed in the right ventricle and an indifferent electrode (8.5-cm diameter plate) sutured to the right chest wall. The catheter electrode was either 0.4 cm or 1.2 cm long and had a surface area of 0.50 cm2 or 1.50 cm2, respectively. A monopolar electrode was positioned at the apex of the right ventricle or midway between the apex and the tricuspid valve. The peak-to-peak amplitude of the pulsatile cardiac-induced impedance change was measured prior to and throughout an episode of ventricular fibrillation lasting up to 1 minute. On the average, the amplitude of the pulsatile RVZ signal after 10 seconds of fibrillation decreased by 79% of the prefibrillation amplitude. The 1.2-cm electrode located at the middle of the ventricle showed the largest reduction in pulsatile impedance, the amplitude being very small at 10 seconds. It is concluded that sensing RVZ by a monopolar electrode located on a catheter in the mid-ventricle can provide the mechanical information needed to identify the onset of ventricular fibrillation.

Animals↗
PubMed2003

Management of ventricular fibrillation or unstable ventricular tachycardia in patients with congenital long-QT syndrome: a suggested modification to ACLS guidelines.

Prolongation of the QT interval is a known risk factor for syncope, seizures and sudden cardiac death. Most patients with QT prolongation have an acquired cause, but congenital forms of QT prolongation are being increasingly recognized. However, existing advanced cardiac life support (ACLS) treatment algorithms for prolonged QT mediated ventricular fibrillation pertains to acquired long-QT syndrome (LQTS). Here, a young patient with out-of-hospital cardiac arrest secondary to congenital LQTS illustrates critical exceptions to the current ACLS treatment algorithms for ventricular fibrillation and unstable ventricular tachycardia when QT prolongation is congenital in origin. A clarified ACLS algorithm is proposed.

Advanced Cardiac Life Support↗
PubMed2000

Dispersion of ventricular repolarization and ventricular fibrillation in left ventricular hypertrophy: influence of selective potassium channel blockers.

This study tested the hypothesis that combination ion channel blockers of the transient outward current (I(to)) and the rapid component of the delayed rectifying current (I(Kr)) would produce greater prolongation of the ventricular action potential duration (APD) and increased dispersion of the APD in hypertrophied hearts compared with control hearts. Isolated rabbit hearts were studied 48 +/- 5 days postabdominal aortic banding. Left ventricular endocardial and epicardial APDs were significantly greater at baseline in the hypertrophied group than in controls (P <.05). The magnitude of APD prolongation induced by the I(to) blocker 4-aminopyridine (4-AP) and combination 4-AP and the I(Kr) blocker dofetilide was greater in the hypertrophied hearts than in the normal hearts (P <.01). Mean APD dispersion was significantly greater in the hypertrophied group than in the control hearts at baseline (P <.05). 4-AP increased APD dispersion by a similar magnitude in the hypertrophied hearts (10 +/- 10 ms) and the control hearts (8 +/- 8 ms, P = NS), whereas the combination 4-AP and dofetilide increased APD dispersion by a greater magnitude in the hypertrophied hearts (41 +/- 28 ms) than the control hearts (21 +/- 11 ms, P <.05). Ventricular fibrillation occurred spontaneously in four hypertrophied hearts (40%) during combination drug perfusion and in none of the control hearts (P <.05). Thus, combination I(to) and I(Kr) blockers cause greater prolongation APD and increased APD dispersion in left ventricular hypertrophy, and this is associated with the development of ventricular fibrillation.

4-Aminopyridine↗
PubMed1981

Ventricular fibrillation complicating temporary ventricular pacing in acute myocardial infarction: significance of right ventricular infarction.

Five patients with acute myocardial infarction had ventricular fibrillation as a complication of indicated temporary pacing. All five patients had evidence of right ventricular infarction (three patients with postmortem confirmation). The presence of right ventricular infarction seems to be a contributing mechanism involved in the induction of ventricular fibrillation during temporary pacing for bradyarrhythmia complicating acute myocardial infarction.

Adult↗
PubMed2002

Mapping and ablation of idiopathic ventricular fibrillation.

BACKGROUND: Ventricular fibrillation is the main mechanism of sudden cardiac death. The feasibility of eliminating recurrent episodes by catheter ablation has not been reported. METHODS AND RESULTS: Twenty-seven patients without known heart disease (13 men, 14 women, 41+/-14 years of age) were studied after being resuscitated from recurrent (10+/-12) episodes of primary idiopathic ventricular fibrillation; 23 had received a defibrillator. The first initiating beat of ventricular fibrillation had an identical electrocardiographic morphology and coupling interval (297+/-41 ms) to preceding isolated premature beats typically noted in the aftermath of resuscitation. These triggers were localized by mapping the earliest electrical activity and ablated by local radiofrequency delivery. Outcome was assessed by Holter and defibrillator memory interrogation. Premature beats were elicited from the Purkinje conducting system in 23 patients: from the left ventricular septum in 10, from the anterior right ventricle in 9, and from both in 4. The interval from the Purkinje potential to the following myocardial activation varied from 10 to 150 ms during premature beat but was 11+/-5 ms during sinus rhythm, indicating location at peripheral Purkinje arborization. The premature beats originated from the right ventricular outflow tract muscle in 4 patients. The accuracy of mapping was confirmed by acute elimination of premature beats during local radiofrequency delivery. During a follow-up of 24+/-28 months, 24 patients (89%) had no recurrence of ventricular fibrillation without drug. CONCLUSIONS: Primary idiopathic ventricular fibrillation is a syndrome characterized by dominant triggers from the distal Purkinje system. These sources can be eliminated by focal energy delivery.

Adult↗
PubMed1999

Beta-blocker use and survival in patients with ventricular fibrillation or symptomatic ventricular tachycardia: the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial.

OBJECTIVES: To evaluate whether use of beta-adrenergic blocking agents, alone or in combination with specific antiarrhythmic therapy, is associated with improved survival in persons with ventricular fibrillation (VF) or symptomatic ventricular tachycardia (VT). BACKGROUND: The ability of beta-blockers to alter the mortality of patients with VF or VT receiving contemporary medical management is not well defined. METHODS: Survival of 1,016 randomized and 2,101 eligible, nonrandomized patients with VF or symptomatic VT followed in the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial through December 31, 1996 was assessed using Cox proportional hazards analysis. RESULTS: The 817 (28%) patients discharged from hospital receiving beta-blockers had less ventricular dysfunction, fewer symptoms of heart failure and a different pattern of medication use compared with patients not receiving beta-blockers. Before adjustment for important prognostic variables, beta-blockade was not significantly associated with survival in randomized or in eligible, nonrandomized patients treated with specific antiarrhythmic therapy. After adjustment, beta-blockade remained unrelated to survival in randomized or in eligible, nonrandomized patients treated with amiodarone alone (n = 1142; adjusted relative risk [RR] = 0.96; 95% confidence interval [CI] 0.64-1.45; p = 0.85) or a defibrillator alone (n = 1347; adjusted RR = 0.88; 95% CI 0.55 to 1.40; p = 0.58). In contrast, beta-blockade was independently associated with improved survival in eligible, nonrandomized patients who were not treated with specific antiarrhythmic therapy (n = 412; adjusted RR = 0.47; 95% CI 0.25 to 0.88; p = 0.018). CONCLUSIONS: Beta-blocker use was independently associated with improved survival in patients with VF or symptomatic VT who were not treated with specific antiarrhythmic therapy, but a protective effect was not prominent in patients already receiving amiodarone or a defibrillator.

Adrenergic beta-Antagonists↗
PubMed2000

[Variable late potentials in long-term ECG of the post-infarct patient at risk for ventricular fibrillation].

BACKGROUND: Ventricular late potentials are found more readily in post-infarction patients who had sustained ventricular tachycardia than in those who survived ventricular fibrillation. Hypothetically, a daytime variability of late potentials might be responsible for this finding. METHOD: Therefore a conventional late potential analysis only performed once a day was compared to a late potential analysis in time and frequency domain repeatedly performed every hour in the Holter-ECG of 160 post-infarction patients (50 patients (= VT-group) with documented, sustained ventricular tachycardia (cycle-length > 230 ms), 50 patients (= VF-group) who survived, documented ventricular fibrillation and 60 patient, without ventricular arrhythmias (= O VT/VF-group)). RESULTS: The conventional analysis showed late potentials in time domain in 72% of the patients in the VT-group, in 40% of patients in the VF-group and in 20% of the patients in the O VT/VF-group. The Holter-ECG showed late potentials to be permanently present in frequency domain in 66% of the patients in the VT-group, in only 6% in the patients in the VF-group and in no patient in the O VT/VF-group. However, in at least one analysis we detected late potentials in 84% of patients of the VF-group, in 90% of patients in the VT-group and in 18% of patients in the O VT/VF-group. Transiently detectable late potentials in patients of the VF-group were predominantly seen at heart rate accelerations in the morning hours, ST-segment shifts or transitory decreased heart rate variability. CONCLUSIONS: Post-infarction patients with sustained ventricular tachycardia predominantly have constantly detectable late potentials over 24 hours. In these patients conventional late potential is successful for post-infarction risk stratification at any time of the day. However, in post-infarction patients who survived ventricular fibrillation, late potentials are found to be transitory and only detectable by Holter-ECG. Thus, late potential analysis performed in the Holter-ECG might improve post-infarction risk stratification in patients prone to sudden cardiac death.

Aged↗
PubMed2005

Atrial fibrillation and recurrent ventricular fibrillation during hypokalemia in Brugada syndrome.

A 41-year-old man with Brugada syndrome (BS) and no previous episodes of aborted sudden death or syncope referred to local emergency room for an episode of symptomatic atrial fibrillation. Blood chemistry results showed hypokalemia (2.9 mEq/L). The other parameters were within the normal range. After few minutes, an episode of ventricular fibrillation treated with biphasic DC shock 150 J occurred. In successive 2 hours, the patient experienced recurrent episodes of ventricular tachycardia and fibrillation. Each biphasic DC shock 150 J was effective to restore sinus rhythm. No further episodes occurred after normalization of serum levels of potassium. Before discharge, an implantable cardioverter defibrillator was inserted to prevent sudden cardiac death. Hypokalemia increases the risk of arrhythmic events in BS.

Adult↗