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PubMed1999

Ventricular fibrillation secondary to ergotamine in a healthy young woman.

A 34-year-old woman collapsed secondary to ventricular fibrillation 3 hours following the ingestion of ergotamine tartrate for migraine. She underwent defibrillation and recovered rapidly without any subsequent consequences. The mechanism of action and the side effects of ergotamine and other antimigraine drugs are discussed. We hypothesize that a coronary spasm induced by ergotamine could be the aetiologic factor leading to ischaemic ventricular fibrillation.

Adult↗

PubMed1999

Syncope and inducible ventricular fibrillation in a woman with hemochromatosis.

BACKGROUND: Hemochromatosis has been associated with atrial tachyarrhythmias and congestive heart failure as a consequence of dilated or restrictive cardiomyopathy. Inducible ventricular fibrillation has not been previously described. METHODS AND RESULTS: An electrophysiologic study was conducted in a woman after two episodes of syncope. Polymorphic ventricular tachycardia (PMVT) and ventricular fibrillation (VF) were induced with ventricular programmed stimulation. Magnetic resonance imaging demonstrated signal loss in the liver consistent with hemochromatosis, but normal cardiac size and function. Hematologic studies supported a diagnosis of hemochromatosis. CONCLUSION: Cardiac hemochromatosis may be associated with serious ventricular arrhythmias.

Echocardiography↗

PubMed1981

[Physiopathologic mechanism of ventricular fibrillation induced by atropine. Report of two cases (author's transl)].

The authors report on two cases of ventricular fibrillation induced by bolus of atropine injected for diagnostic purpose. The electrophysiologic effect of adrenergic stimulation following the parasympathetic blockade, is probably the responsible mechanism rather than myocardial ischemia in the first patient, affected by complete a-v block with narrow QRS. The second patient, affected by coronary heart disease and suspected sick sinus syndrome, had more probably a ventricular fibrillation because of a worsening of the underlying myocardial ischemia due to the increase of the cardiac rate. the reported observations, together with those of other Authors, suggest that atropine, at least when used for diagnostic purpose, should be employed cautiously and preferably having available all the equipment for emergency treatment of cardiorespiratory arrest.

Aged↗

PubMed2004

Presence of intermittent J waves in multiple leads in relation to episode of atrial and ventricular fibrillation.

Brugada syndrome is characterized by J wave and ST-segment elevation of right precordial leads and causes idiopathic ventricular fibrillation. We experienced a patient of Brugada syndrome with prominent J wave and ST-segment elevation not only in V(1) to V(3) but also in many leads. He suffered spontaneous ventricular fibrillation and resuscitated by direct current. He has no structural heart disease.

Atrial Fibrillation↗

PubMed1983

The use of bretylium in prehospital ventricular fibrillation.

Bretylium tosylate is recommended by the American Heart Association Standards for Advanced Cardiac Life Support for refractory ventricular fibrillation after countershock, sodium bicarbonate, and epinephrine. According to this protocol, paramedics gave five to six milligrams per kilogram of intravenous bretylium by bolus in 96 patients with refractory fibrillation over a 24-month period. A positive response was defined as the presence of a palpable pulse following bretylium and countershock. Thirty-five percent of patients (34/96) responded following bretylium. Twenty-one percent (20/96) responded only temporarily with a rhythm and pulse. Fifteen percent (14/96) maintained a stable rhythm and vital signs on admission to the hospital, but only five patients, 5% of the total population, (5/96), were eventually discharged home. Clinical variables were similar in non-responders, temporary responders, and those admitted, but the times from the onset of Advanced Cardiac Life Support to receiving bretylium were 23.5 min, 20.3 min, and 14.3 min respectively. We conclude that about one-third of patients in refractory ventricular fibrillation respond following bretylium and countershock and that earlier bretylium use may give better results.

Bretylium Compounds↗

PubMed1983

Disopyramide: evaluation of electrophysiologic effects and clinical efficacy in patients with sustained ventricular tachycardia or ventricular fibrillation.

The efficacy of disopyramide in the management of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) was evaluated in 50 patients by programmed ventricular stimulation: 38 patients had coronary artery disease (16 with left ventricular aneurysm), 8 had other cardiac diseases, and 4 had no apparent heart disease. Disopyramide was administered orally for 72 hours (dosage 400 to 1,600 mg/day), resulting in a plasma level of 3.6 +/- 1.2 micrograms/ml (mean +/- standard deviation [SD]). Disopyramide prevented induction of sustained ventricular tachyarrhythmias in 17 patients (34%) and failed to prevent induction in 33 patients (66%). Plasma levels were not significantly different regardless of response to disopyramide. The VT cycle length in patients responding to disopyramide was shorter than in nonresponding patients (225 +/- 51 ms versus 281 +/- 70 ms, p = 0.005). Disopyramide increased VT cycle length in those patients in whom it was ineffective (failed to prevent induction) from 281 +/- 70 ms to 347 +/- 64 ms (p less than 0.001). Ventricular refractory periods, QRS, and QTc durations significantly increased after disopyramide administration. Of the 17 patients in whom tachyarrhythmias were noninducible on disopyramide, 11 were discharged on disopyramide and followed up for 19 +/- 9 months; 9 of them remained free of VT. Heart failure developed in 2 of these patients. One other patient in whom disopyramide was ineffective had irreversible heart failure and died. It is concluded that disopyramide (1) prevents induction of ventricular tachyarrhythmias in one third of patients studied and remains clinically effective in approximately 80%, (2) is more frequently effective in rapid tachycardias, (3) prolongs the VT cycle length when ineffective, and (4) may produce marked hemodynamic embarrassment in patients with significant left ventricular dysfunction.

Adult↗

PubMed1995

Antifibrillary action of class I-IV antiarrhythmic agents in the model of ventricular fibrillation threshold of anesthetized guinea pigs.

We compared the effects of class I-IV antiarrhythmic agents on the ventricular fibrillation threshold (VFT) induced by electrical stimulation directly on the myocardium in anesthetized, open-chest guinea pigs. VFT was assessed by determining the intensity (mA) of electrical current required to induce ventricular fibrillation (VF) and is expressed as a percentage change of the baseline premedication value. The following antiarrhythmic agents or their solvent were administered intravenously (i.v.) to pentobarbital-anesthetized animals (n = 6-12 per group): class I antiarrhythmic agent encainide (1.5 mg/kg); class II antiarrhythmic agents atenolol (2.5 mg/kg), metoprolol (2.5 mg/kg), and nebivolol (2.5 mg/kg); class III antiarrhythmic agents dofetilide (0.08 mg/kg), terikalant (0.04 mg/kg), and DL-sotalolol (10 mg/kg); and class IV antiarrhythmic agent verapamil (0.16 mg/kg). The antiarrhythmic compounds or their solvents resulted in the following changes in the VFT at 15 min after treatment: saline control, 1 +/- 14% (mean +/- SEM) from its baseline value; 10% hydroxypropyl-beta-cyclodextrine (CD), 4 +/- 13%; encainide, 183 +/- 46% (p < 0.05 vs. saline); atenolol, 66 +/- 23% (p > 0.05 vs. saline); metoprolol, 89 +/- 25% (p > 0.05 vs. saline); nebivolol, 224 +/- 58% (p < 0.05 vs. 10% CD); DL-sotalol, 485 +/- 119% (p < 0.05 vs. saline); dofetilide, 357 +/- 69% (p < 0.05 vs. saline); terikalant, 487 +/- 183% (p < 0.05 vs. saline), and verapamil, -17 +/- 21% (p > 0.05 vs. saline). At the doses used, all compounds significantly reduced heart rate (HR).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed2002

Ventricular fibrillation: ablation of a trigger?

We report the case of a patient with recurrent ventricular fibrillation (VF) and no evidence of structural heart disease. VF was consistently initiated by a relatively early-coupled premature ventricular contraction with identical morphology on each occasion. Treatment with antiarrhythmic agents failed to suppress the arrhythmia. Electrophysiologic testing showed high-frequency potential at the earliest activation site, and radiofrequency ablation resulted in abolition of the ventricular ectopy with no further VF recurrence. Suppression of VF arising from focal triggers in patients with frequent ventricular ectopy and normal heart can be achieved with catheter ablation, but further studies are needed to evaluate the prevalence of such a mechanism.

Adult↗

PubMed1982

Ventricular fibrillation after intravenous atropine in a patient with atrioventricular block.

A 69-year-old black woman with complete AV block developed ventricular fibrillation following an IV injection of 1 mg of atropine sulphate. After a successful DC countershock, the ECG showed a polymorphous ventricular tachycardia which subsided spontaneously. Cardiac catheterization revealed a small left ventricular diverticulum and normal coronary arteries. This seems to be the first reported case of atropine-induced ventricular fibrillation in a patient with complete AV block. The fact that this occurred without previous change of the ventricular rate suggests that the adverse action of atropine was mediated through a mere vagolytic effect at the ventricular level.

Aged↗

PubMed2005

Effect of remodelling, stretch and ischaemia on ventricular fibrillation frequency and dynamics in a heart failure model.

OBJECTIVE: The dynamics of ventricular fibrillation (VF) in the presence of heart failure (HF) are different from those in the normal heart. This has been attributed solely to HF-induced electrophysiologic remodelling. We hypothesized that acute stretch and ischaemia, which are normally present during VF, might contribute significantly to the altered VF dynamics in HF. METHODS: HF was induced in eight sheep by rapid ventricular pacing for 4-6 weeks. Eight sheep served as controls. Optical mapping of isolated hearts was performed during VF at low intraventricular pressure (0-5 mm Hg), high pressure (25-30 mm Hg, in six HF and six controls), and at low pressure after 5 min of global ischaemia (six HF, five controls). Maximum dominant frequency (DF(max)), singularity point (SP) density and number of SP lasting more than one revolution (rotors) were analyzed. Possible statistical interactions between HF and ischaemia (HF x ischaemia) or stretch (HF x stretch) were evaluated. RESULTS: At low pressure, VF in HF was slower (13% reduction in DF(max)) and more organized than in control: 33% less SPs and 74% less rotors with 20% longer life spans. Acute stretch did not affect DF(max) but increased SP and rotors density similarly in both groups (no interaction HF x stretch). In controls, ischaemia caused a marked decrease in DF(max), SP density and incidence of rotors. However, in HF animals, the ischaemia-induced decrease in SP density was virtually abolished, indicating a significant interaction HF x ischaemia (p<0.005). CONCLUSIONS: HF remodelling decreases VF rate and increases VF organization. Acute stretch partially reverses these effects by a mechanism that is independent of remodelling. The effects of acute ischaemia on VF dynamics are significantly attenuated in HF compared to normal hearts.

Action Potentials↗

PubMed1986

Prevention of postischaemic ventricular fibrillation by long term beta adrenoceptor blockade with acebutolol in the anaesthetised dog.

Acute occlusions of the proximal left circumflex coronary arteriovenous pedicle were performed in open chest anaesthetised dogs. Twenty eight dogs were randomly allocated to receive acebutolol (3 mg X kg-1 twice daily) or placebo given blindly by mouth for five days; a control group of 14 dogs without any pretreatment underwent the same procedure. Coronary ligations in the randomised study were performed during seven consecutive days, and four dogs were operated on each day. This schedule was chosen in order to measure acebutolol plasma concentrations just before ligation from 60 to 540 min after the last dose of the drug. Long term oral treatment with acebutolol protected against postischaemic ventricular fibrillation and significantly reduced the incidence of both early phase (0-10 min postocclusion) ventricular arrhythmias and ventricular fibrillation. As a result the outcome was significantly improved after 60 min of ischaemia in acebutolol compared with placebo treated animals. The results in the control animals were similar to those in the placebo treated dogs. The protective effect of long term oral treatment with acebutolol lasted for nine hours and was apparently independent of the plasma concentrations of the drug. These data show that improved outcome in this canine model is due to the prevention of ischaemia induced ventricular fibrillation by long term beta adrenoceptor blockade, which is able to overcome the effect, if any, of partial agonist activity of acebutolol. A direct myocardial anti-ischaemic effect might explain the effectiveness of long term oral treatment, which is independent of plasma concentrations of the drug.

Acebutolol↗

PubMed1975

[Syncopal attacks and sudden death due to ventricular fibrillation -- a variant of the Jervell or Lange-Nielsen syndrome (author's transl)].

Syncopal attacks due to ventricular fibrillation or -- flutter with elongation of QT in the ECG and deafness are signs of a congenital condition described by Jervell and Lange-Nielsen 18 years ago. Since then we have learned that the range of variation of symptoms is very wide. There are differences genetically and in age-groups. A boy aged 15 years with supposedly cerebral fits is reported on. Since the right diagnosis was missed he had been treated with anticonvulsants for years. But these were syncopal attacks, Effort produced a tendency to bigeminus. -- A knee-bending exercise repeated 13 times lead to his death from ventricular fibrillation. Post-mortem examination showed no pathologic findings except mild left hypertrophy of the ventricle. His sister also had similar attacks without spasms after excitement or mild physical effort. She too had no extension of the QT interval. Their mother and grandmother also had syncopal attacks and died at the ages of 31 and 24 years. A girl-cousin died suddenly at the age of 15. In addition we have seen a neonate with a mild cardiac murmur on whom an ECG was done on the 16th day. The QT interval was significantly prolonged. There were numerous extrasystoles. He died suddenly 2 days later. Post mortem showed no cardiac pathology. One should now be able to explain some cases of unexpected natural death. But ignorance of the pathogenesis does not yet permit definition of the clinical pictures.

Adolescent↗

PubMed2002

Terikalant and barium decrease the area of vulnerability to ventricular fibrillation induction by T-wave shocks.

The area of vulnerability (AOV) to ventricular fibrillation (VF) induction by high-voltage shocks has been proposed as a measure of vulnerability to VF. Biphasic shocks spanning the T wave and ranging between 50 V and the upper limit of vulnerability (ULV) to VF were delivered before and after terikalant (1 mg/kg) and barium (1.1 mg/kg load followed by 0.05-0.10 mg/kg/min maintenance) or vehicle in dogs. The AOV decreased by 34% and 28% (p < 0.01) after terikalant and barium (n = 8 dogs each), respectively. Mean ULV, defibrillation threshold (DFT), and ventricular vulnerability period (VVP) decreased by 16%, 23%, and 31% (p < 0.01), respectively, after terikalant, and by 25%, 17% (p < 0.01), and 13% (p = 0.08), respectively, after barium. Vehicle (n = 14) did not significantly alter any of these variables. The ULV was correlated with the DFT before and after terikalant (r = 0.78, p < 0.01) and barium (r = 0.83, p < 0.01). Potassium channel blockers of the current reduce the ability to induce VF; this effect may be related to the anti-fibrillatory action of class III anti-arrhythmic drugs and their ability to decrease DFT.

Action Potentials↗

PubMedDate not supplied

Contrast media induced ventricular fibrillation during coronary angiography in dogs.

This study is designed to determine which is more critical for contrast media induced ventricular fibrillation (VF), hyperosmolality or lack of sodium ions. The right coronary artery in the canine model was infused continuously with contrast media (CM) for 25 seconds or until ventricular fibrillation occurred. The test solutions included isotonic saline, 305 mg I/ml of meglumine diatrizoate, 370 mg I/ml of meglumine/Na diatrizoate and 370 mg I/ml of metrizamide. The incidence of VF with meglumine/Na diatrizoate was significantly higher than with metrizamide (p less than 0.05). These observations suggest that the hyperosmolality is more critical than the lack of sodium ions in CM when metrizamide is compared with conventional ionic CM. On the other hand, the results showing that contact time until VF was shorter with meglumine diatrizoate than with meglumine/Na diatrizoate may reflect the importance of sodium ions in CM with similar osmolality.

Animals↗

PubMedDate not supplied

Decreased incidence of ventricular fibrillation after an acute coronary artery ligation in exercised pigs.

Evidence has been presented that regular physical activity may be associated with a decreased incidence of sudden cardiac death. It has been suggested that self-selection of those engaging in regular exercise rather than the physical activity itself is a major factor in explaining these results. We therefore studied the effects of a two-month exercise program on the incidence of ventricular fibrillation after an acute ligation of the left anterior descending (LAD) coronary artery in domestic Yorkshire pigs. At the end of the exercise program, the exercised group (EG, n = 17) had a lower heart rate (10%), a 5 times higher maximum exercise capacity, a 10% larger left ventricular mass and a thicker myocardial wall during end-diastole than a sedentary group (SG, n = 13). After the animals were anesthetized, the LAD artery was occluded at one third of its distal end. Ventricular fibrillation (VF) occurred in 92% of the SG (12 out of 13) against only 30% of the EG (5 out of 17) within 1 hour after occlusion. Percentage of the area at risk was the same (9-10% of total left ventricular mass) in both the EG and SG. Transmural myocardial perfusion after coronary artery ligation was slightly larger in EG than in SG (30 vs 21 ml . min-1 . 100 g-1, p less than 0.05). Although the improvement in perfusion of the ischemic zone of the EG may have contributed to the reduced occurrence of ventricular fibrillation, other mechanisms cannot be excluded.

Acute Disease↗

PubMedDate not supplied

Automated external defibrillators appropriately recognize ventricular fibrillation in electromagnetic fields.

OBJECTIVES: Automated external defibrillators (AEDs) are increasingly available in industrial settings, but many industries have high electromagnetic fields (EMFs), which can interfere with the function of electronic devices. This study evaluated the performance of several AEDs when exposed to high EMFs. METHODS: Three commercially available AEDs were evaluated in the setting of a public utility coal-fired electrical generation plant. Each AED was placed in three areas of high EMF ranging from 310 to 1,600 milligauss. A signal generator, used to simulate various cardiac rhythms, was connected to the AEDs. Rhythms simulated were ventricular fibrillation, asystole, and normal sinus rhythm. Each of the AED's interpretations of various rhythms were evaluated in the different EMF settings. RESULTS: Rhythms of ventricular fibrillation, asystole, and normal sinus rhythm were correctly recognized by each AED in each of the three areas of high EMF. Each AED appropriately recommended defibrillation when presented with ventricular fibrillation. No misinterpretations or inappropriate defibrillations were observed. CONCLUSION: Electromagnetic fields generated by an electrical power plant did not interfere with three commercial AEDs' abilities to correctly interpret simulated rhythms and recommend appropriate defibrillation.

Cardiopulmonary Resuscitation↗

PubMed1987

Effects of Sophora flavescens Ait. on haemodynamics and ventricular fibrillation threshold in anaesthetized dogs.

The effects of an ethanol extract of the plant Sophora flavescens Ait. on haemodynamics and ventricular fibrillation threshold were studied in pentobarbitone-anaesthetized dogs. It was found that intravenous injection of the extract, 120 mg/kg, caused transient but significant depression in systolic and diastolic blood pressure, heart rate, left ventricular pressure and dLVP/dtmax, as well as elevation of ventricular fibrillation threshold. These preliminary findings suggest that the ethanol extract of Sophora flavescens Ait. possesses pharmacological activities resembling those of antiarrhythmic agents, but the mechanisms of action are unclear.

Anesthesia, Intravenous↗

PubMed1988

Comparative effects of antiarrhythmic drugs on the ventricular fibrillation threshold.

The purpose of this study was to compare the effects of several different antiarrhythmic drugs on the ventricular fibrillation threshold (VFT). Experiments were performed on open-chest dogs anesthetized with pentobarbital. The VFT was measured on the right ventricle by scanning the vulnerable period with a single 10-ms electrical stimulus. The following antiarrhythmic drugs were each given intravenously to eight different dogs: procainamide (25 mg/kg), lidocaine (2 mg/kg + 70 micrograms/kg/min), flecainide (3 mg/kg), timolol (0.1 mg/kg), clofilium (1 mg/kg), dl-sotalol (5 mg/kg), and bethanidine (4 mg/kg). The drugs resulted in the following increases in the VFT: procainamide, 33 +/- 13%; lidocaine, 21 +/- 5%; flecainide, 38 +/- 10%; timolol, 19 +/- 6%; clofilium, 14 +/- 6%; sotalol, 33 +/- 10%; and bethanidine, 69 +/- 15%. The changes in VFT were all significant (p less than 0.01) except for clofilium. Only procainamide and sotalol caused stimulus-induced runs of nonsustained polymorphic ventricular tachycardia that spontaneously reverted to sinus rhythm after 4 s or more. In individual experiments, the occurrence of nonsustained polymorphic tachycardia that resembled ventricular fibrillation could not be correlated with a change in the VFT. In addition, there appeared to be no relationship between a drug-induced increase of the VFT and alterations in the QRS duration, the QT interval, or the ventricular effective refractory period. Bethanidine had the greatest effect on the VFT, in spite of the fact that this drug shortened the ventricular effective refractory period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗