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At least 811 records · Page 45Linked to original sources
PubMed1991

Diazepam administered prior to coronary artery occlusion increases latency to ventricular fibrillation.

Few studies have addressed the antiarrhythmic potential of pretreatment with diazepam in acute myocardial infarction. Thus, the effect of diazepam pretreatment prior to coronary artery occlusion was examined in conscious pigs. Animals were instrumented with aortic catheters to measure arterial pressure, a pulmonary artery catheter for drug administration, and a snare around the left anterior descending coronary artery for permanent occlusion one week later. Diazepam (1 mg/kg iv bolus) or vehicle was administered 10 minutes prior to occlusion. Eight of 14 animals receiving diazepam (57%) and 13 of 22 receiving vehicle animals (59%) developed ventricular fibrillation following coronary occlusion. However, the latency to ventricular fibrillation was significantly shorter (7 +/- 1 min) in animals receiving vehicle compared to animals receiving diazepam (11 +/- 1 min). Significant increases in heart rate were seen up to 5 hours after coronary occlusion only in animals receiving vehicle. The results indicate that diazepam pretreatment can increase ventricular fibrillation latency and prevent heart rate increases following acute myocardial infarction.

Animals↗
PubMed1978

Thiazide-induced hypokalemia. Association with acute myocardial infarction and ventricular fibrillation.

Ten of 59 patients (17%) were receiving a thiazide preparation at the time of an acute myocardial infarction and ventricular fibrillation. Hypokalemia was present in seven of eight patients (87%) receiving thiazides, whereas it was observed in only one of 38 patients (2.6%) not receiving these medications. If hypokalemia is present in patients receiving thiazides who have had an acute myocardial infarction, it should be corrected so as to remove this predisposing cause of ventricular fibrillation.

Acute Disease↗
PubMed1992

[Effects of bonnecor on transmembrane potentials of cardiomyocytes of the ventricular contractile myocardium of the intact heart and ventricular fibrillation].

The microelectrode technique has shown that bonnecor given in a dose of as many as 2 mg/kg increases the action potential amplitude, but when its dose is increased up to 3 mg/kg, the agent decreases the action potential amplitude of ventricular cardiomyocytes in the guinea-pig, the resting potential remaining steady. Administration of bonnecor prevents ventricular fibrillation after aconitine application and provokes ventricular fibrillation and flutter when the focus of ectopic automatism is formed.

Animals↗
PubMed2001

Core rewarming via warm lavage liquid ventilation in a swine model of hypothermia-associated ventricular fibrillation.

OBJECTIVES: To determine whether warm lavage liquid ventilation (LV) would provide rapid cardiopulmonary rewarming in swine with severe hypothermia and ventricular fibrillation. METHODS: Intubated common swine (n = 3; mean +/- SEM weight 26+/-1.2 kg) were cooled to a mean aortic temperature of 26.4+/-0.9 degrees C. Ventricular fibrillation was induced by transthoracic electrical shock. Rewarming was initiated by continuous endotracheal instillation of warm (44 degrees C) pre-oxygenated, perfluorocarbon liquid at 5 mL/kg/min. Endotracheal instillation of perfluorocarbon occurred while standard gas ventilation continued. Manual chest compressions were performed throughout the 30-minute rewarming process. Outcome measures were the absolute and relative rates of change of all temperatures. RESULTS: After 30 minutes of warm lavage LV, the mean aortic and pulmonary artery temperatures increased by 6.6+/-0.6 degrees C, respectively. Esophageal, nasal, and rectal temperatures did not change significantly. In one animal, normal sinus rhythm spontaneously returned after 16 minutes of rewarming. CONCLUSIONS: During cardiac arrest, warm lavage liquid ventilation may produce rapid cardiopulmonary rewarming.

Analysis of Variance↗
PubMed2001

Ventricular fibrillation during off-pump coronary artery bypass grafting: transcranial Doppler and clinical findings.

A 73-year-old male developed ventricular fibrillation which lasted for 2 min and 24 s, during off-pump coronary artery bypass grafting. Cerebral hemodynamics were assessed by continuous transcranial Doppler monitoring. Ventricular fibrillation resulted in an immediate fall in cerebral blood flow velocities to almost zero with only slight fluctuations. This was then followed by a pronounced reactive hyperperfusion. Cerebral magnetic resonance imaging examinations and detailed neurological and neuropsychological evaluations were performed before and at 3 and 12 months after surgery. No evidence of cerebral damage was found.

Aged↗
PubMed1978

[Ventricular fibrillation under quinidine medication--quinidine syncope (author's transl)].

Ventricular fibrillation which may occur unexpected under quinidine medication--called quinidine syncope--is one of the most dangerous complications of quinidine application. These life threatening accidents occur in 0,5-4,4% treated cases. The quinidine syncope occurs mostly at the attempt to eliminate atrial fibrillation or flutter. This dangerous side effect is dose independent. The ECG shows an increased QT duration and large U-waves. It seems to be a reentry-tachycardia caused by unequal recovery times in different parts of the ventricular myocardium.

Digitoxin↗
PubMed1987

Ventricular fibrillation survivors in whom tachyarrhythmia cannot be induced: outcome related to selected therapy.

Eight-five patients were studied to determine the prognosis of the ventricular tachyarrhythmias at the time of electrophysiologic study. Twenty-five patients (29%) were not inducible when we used a stimulation protocol consisting of up to four extrastimuli delivered at two right ventricular sites. Patients with no inducible arrhythmias were younger (53 vs 59 yrs; p = .06) and had higher ejection fractions (.49 vs .34; p less than .04) than the inducible ventricular fibrillation survivors. Sex, cardiac diagnosis, time from event to electrophysiologic study, and antiarrhythmic therapy at the time of event did not discriminate between those with and those without inducible ventricular tachyarrhythmias. Survival free of recurrent sudden death or ventricular tachycardia was .86 +/- .05 and .95 +/- .05 for patients with and without inducible tachyarrhythmias, respectively (p = .22). Nine of 25 (36%) patients with no inducible arrhythmias developed inducible ventricular tachyarrhythmias when testing was repeated with an antiarrhythmic drug. Ventricular fibrillation survivors not inducible at the time of programmed ventricular stimulation (using a stimulation protocol consisting of four extrastimuli delivered at two right ventricular sites) seem to have a good prognosis. Many "noninducible" patients develop inducible tachyarrhythmias when placed on antiarrhythmic therapy. Because it is possible that these drugs are proarrhythmic, empiric antiarrhythmic therapy should be avoided in these patients.

Adult↗
PubMed1994

Survival in patients found to have ventricular fibrillation after cardiac arrest witnessed outside hospital.

Since 1980 an Emergency Medical Service (EMS) system with a two-tier ambulance service has been operating in Göteborg. During this 12-year period, all cardiac arrests outside hospital have been monitored. Cardiopulmonary resuscitation (CPR) training for the general public began in 1985 and, by the end of 1992, 125 000 persons had been trained. The aim of this study was to define the factors associated with an increased chance of survival after cardiac arrest witnessed out-of-hospital and secondary to ventricular fibrillation. The study group comprises all patients with cardiac arrest witnessed outside hospital in Göteborg between 1980 and 1992, in whom CPR was initiated by our EMS and ventricular fibrillation observed at the first ECG recording. In a multivariate analysis of age, sex, time of collapse, interval between collapse and first defibrillation, bystander-initiated CPR, the following factors were associated with an increased chance of being discharged from hospital: (1) Short interval between collapse and first defibrillation (P < 0.001); (2) Bystander-initiated CPR (P < 0.001); and (3) Age (P < 0.05). Among patients with an out-of-hospital cardiac arrest who were found by the EMS personnel to have ventricular fibrillation, the predictors of survival were: interval between collapse and defibrillation, bystander-initiated CPR and age.

Adolescent↗
PubMed1985

[Classification of ventricular fibrillation].

The authors analyse the most common classifications of ventricular fibrillation. Indicate that agonal fibrillation should not be distinguished. Suggest a modified classification and explain the necessity of introducing some changes into the classification.

Death↗
PubMed1983

Effects of dazoxiben on arrhythmias and ventricular fibrillation induced by coronary artery occlusion and reperfusion in anaesthetised greyhounds.

1 The effects of the thromboxane synthetase inhibitor dazoxiben (UK 37248) on haemodynamics, blood gases, thromboxane and prostacyclin release and on arrhythmias were examined in anaesthetised greyhounds subject to acute coronary artery occlusion and reperfusion. 2 Ten minutes after the administration of UK 37248 2 mg/kg intravenously, the plasma concentration of thromboxane B2 in the coronary sinus was significantly reduced whereas the 6-keto-prostaglandin F1 alpha concentration was increased. 3 UK 37248 did not significantly alter the number of arrhythmias or the incidence of ventricular fibrillation resulting from coronary artery occlusion. There was evidence, however, that in some drug-treated animals there may have been incomplete inhibition of thromboxane synthesis during coronary artery occlusion. 4 A further dose of 1 mg/kg UK 37248 was administered intravenously 5 min before the release of the 40 min coronary artery occlusion. Seven out of eight control dogs died in ventricular fibrillation following reperfusion whereas only one out of eight drug-treated animals fibrillated. 5 This latter result suggests that thromboxane may be an important factor in reperfusion induced ventricular fibrillation and that dazoxiben may be a useful drug in clinically related situations.

Anesthesia↗
PubMed1999

Implantable devices versus antiarrhythmic drug therapy in recurrent ventricular tachycardia and ventricular fibrillation.

The implantable cardioverter defibrillator (ICD) protects patients from sudden cardiac death due to ventricular tachyarrhythmias. The capability of an improved overall survival of high-risk patients in comparison to the best pharmacologic therapy has been evaluated over the last few years in prospective randomized trials. In patients with a history of resuscitated ventricular fibrillation (VF) or unstable ventricular tachycardia (VT), the ICD was superior to therapy with amiodarone in 3 large trials involving 2,024 patients. At 2-year follow-up, ICD therapy was associated with a relative reduction in the risk of death of 20% to 30%. With respect to primary prevention of arrhythmogenic death, data are less convincing. The Multicenter Automatic Implantable Defibrillator (MADIT) study proved superiority of ICD therapy over medical treatment in coronary patients with depressed left ventricular function, nonsustained VT, and inducible but not suppressible sustained VT/VF. The second trial, the Coronary Artery Bypass Graft (CABG)-Patch trial, failed to show a similar superiority in 900 patients with an ejection fraction of < or = 35% and an abnormal signal-averaged electrocardiograph undergoing coronary artery bypass grafting. Thus, the role of device therapy for primary prevention of sudden death has not been established. Future prospective studies are needed to clarify this issue.

Amiodarone↗
PubMed1998

Electrocardiographic identification of abnormal ventricular depolarization and repolarization in patients with idiopathic ventricular fibrillation.

OBJECTIVES: We sought to gain more insight into the arrhythmogenic etiology of idiopathic ventricular fibrillation (VF) by assessing ventricular depolarization and repolarization properties by means of various electrocardiographic (ECG) techniques. BACKGROUND: Idiopathic VF occurs in the absence of demonstrable structural heart disease. Abnormalities in ventricular depolarization or repolarization have been related to increased vulnerability to VF in various cardiac disorders and are possibly also present in patients with idiopathic VF. METHODS: In 17 patients with a first episode of idiopathic VF, 62-lead body surface QRST integral maps, QT dispersion on the 12-lead ECG and XYZ-lead signal-averaged ECGs were computed. RESULTS: All subjects of a healthy control group had a normal dipolar QRST integral map. In patients with idiopathic VF, either a normal dipolar map (29%,), a dipolar map with an abnormally large negative area on the right side of the thorax (24%) or a nondipolar map (47%) were recorded. Only four patients (24%) had increased QT dispersion on the 12-lead ECG and late potentials could be recorded in 6 (38%) of 16 patients. During a median follow-up duration of 56 months (range 9 to 136), a recurrent arrhythmic event occurred in 7 patients (41%), all of whom had an abnormal QRST integral map. Five of these patients had late potentials, and three showed increased QT dispersion on the 12-lead ECG. CONCLUSIONS: In patients with idiopathic VF, ventricular areas of slow conduction, regionally delayed repolarization or dispersion in repolarization can be identified. Therefore, various electrophysiologic conditions, alone or in combination, may be responsible for the occurrence of idiopathic VF. Body surface QRST integral mapping may be a promising method to identify those patients who do not show a recurrent episode of VF.

Adult↗
PubMed1977

Positive radionuclide myocardial infarction pattern after ventricular fibrillation and direct current countershock.

A patient is presented in whom direct current counter-shock was applied for primary ventricular fibrillation. He recovered uneventfully and no evidence was found of a myocardial infarction; however, a positive 99m technetium stannous diphosphate scan obtained four days after the defibrillation showed positive findings. This positive scintigram was most probably due to myocardial or skeletal muscular damage consequent to counter-schock, but myocardial necrosis induced by ventricular fibrillation may be another cause. This case demonstrates again that a transmural or subendocardial infarction is not the only circumstance under which an abnormal scintigram can be obtained.

Electric Countershock↗
PubMedDate not supplied

Relationships between the severity of myocardial ischaemia, reperfusion-induced ventricular fibrillation, and the late administration of dazmegrel or nifedipine.

We examined the effects of late administration of the thromboxane synthetase inhibitor dazmegrel (UK 38485) and the calcium channel blocker nifedipine in anaesthetised greyhounds subject to occlusion of the left anterior descending coronary artery with reperfusion after 40 min of ischaemia. Administration of dazmegrel, 3 mg/kg i.v., or nifedipine, 5 micrograms/kg + 1 microgram kg-1 min-1 i.v., 25 min after coronary artery occlusion failed to reduce the incidence of reperfusion-induced ventricular fibrillation (controls, 70%; dazmegrel, 50%; nifedipine, 70%; n = 10). Measurement of plasma prostanoid concentrations indicated that within 5 min of receiving dazmegrel there was a significant reduction in thromboxane B2 concentrations in the local coronary vein draining the ischaemic myocardium. The results suggest that the occurrence of reperfusion-induced ventricular fibrillation depends upon the severity of changes occurring during ischaemia. Analysis of various factors suggested that the number of ischaemia-induced arrhythmias, heart rate, and the magnitude of changes in local coronary venous PO2 may be important predictors of reperfusion-induced ventricular fibrillation.

Animals↗
PubMed1998

Probability of induction and stabilization of ventricular fibrillation with epinephrine.

Clinical studies suggest that epinephrine facilitates ventricular fibrillation (VF) although mechanisms remain unclear. We tested the hypothesis that epinephrine increases the probability of inducing VF and stabilizes VF in association with shortening of fibrillation action potential duration. VF was induced in isolated, New Zealand White rabbit hearts (n=16) under control conditions and in the presence of 0.9 micro M/l epinephrine. Monophasic action potentials were recorded during sinus rhythm, pacing, and fibrillation. Epinephrine reduced fibrillation p80 by 80%, from 23+/-4 to 4.6+/-1 V (P<0.05); and reduced fibrillation p90 by 82%, from 29.3+/-5.4 to 5.4+/-1.9 V (P<0.05). Epinephrine also reduced the probability of spontaneous termination of VF during the first 5 s of VF from 29 to 8% (P<0.05). Epinephrine significantly decreased mean fibrillation cycle length from 104.5+/-2 to 75.7+/-2.3 ms (P<0.001). Mean action potential duration (60% repolarization) decreased from 76+/-3 to 40+/-3 ms (P<0.0003). Frequency analysis showed a mean dominant frequency during VF of 10.0+/-0.2 Hz under control conditions and 13. 3+/-0.3 Hz with epinephrine (P<0.0001). These results suggest that epinephrine increases the probability of VF induction and decreases the probability of spontaneous defibrillation. Stabilization of fibrillation is associated with shortening of action potential duration and fibrillation cycle length, which may allow a greater number of fibrillation waves in the ventricle.

Action Potentials↗
PubMed1993

[Primary ventricular fibrillation].

In the absence of autopsy studies, the etiological diagnosis of this form of ventricular fibrillation (VF) depends on the exclusion of cardiac disease by all available invasive and non-invasive diagnostic methods. Primary VF is rare and affects young adults. There are few clinical markers and published electrophysiological data indicates that sustained ventricular tachycardia or VF is unlikely to be induced by programmed ventricular stimulation. The underlying mechanism of the arrhythmia is poorly understood. However, a possible arrhythmogenic substrate has been suggested in small zones of fibrosis within normal Purkinje tissues, as encountered in some minor forms of arrhythmogenic right ventricular dysplasia. Also, the role played by the autonomic nervous system in triggering VF seems to be particularly important. Some described cases resemble curiously "torsades de pointes" with a short coupling interval. The "cardiac" prognosis of resuscitated patients is usually good. However, arrhythmic recurrences are common, and, classically, antiarrhythmic drugs are usually ineffective. The indication for implantation of an automatic defibrillator is therefore justified in patients surviving primary VF. The lack of understanding of this condition is an argument in favour of setting up a French register of patients with primary VF in order to establish its clinical features.

Arrhythmias, Cardiac↗