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At least 19 recordsLinked to original sources
PubMed1978

A chronically implanted system for automatic defibrillation in active conscious dogs. Experimental model for treatment of sudden death from ventricular fibrillation.

Ventricular defibrillation was acheived in active conscious dogs with a chronically implanted automatic system composed of a defibrillator and an alternating current fibrillator. The hermetically sealed defibrillator is encased in titanium, weighs 250 g and has a volume of 145 ml. The sensor continuously monitors ventricular electircal activity and recognizes fibrillation by the absence of isoelectric potential segments. Fibrillation is induced by placing a magnet over the implanted fibrillator. The resulting syncope closely resembles the clinical entity of sudden death, while the defibrillator automatically restores normal rhythm with a truncated exponential pulse of 30 J, 15 seconds after the onset of the arrhythmia. The operational status of the defibrillator can be tested in vitro and noninvasively in vivo with an external analyzer. This experimental model allows for the first time a long-term study of the automatic implantable defibrillator approach to prevent sudden death from ventricular fibrillation under a variety of physiopathologic conditions.

Animals↗
PubMed1978

Ventricular fibrillation during programmed ventricular stimulation: incidence and clinical implications.

Ventricular fibrillation occurred in 10 (3.3 percent) of 300 patients consecutively studied with programmed ventricular stimulation. One hundred twenty-five of these patients were studied with double ventricular extrastimuli including 68 patients with and 57 patients without documented or suspected ventricular tachycardia or fibrillation, or both. Ventricular fibrillation did not develop in response to a single ventricular extrastimulus delivered during sinus rhythm, ventricular pacing or ventricular tachycardia or in response to ventricular pacing at cycle lengths of 300 msec or greater and occurred only in response to double ventricular extrastimuli. All 10 patients who manifested ventricular fibrillation during programmed stimulation were in the group of patients with suspected or documented ventricular tachycardia or fibrillation. Ventricular fibrillation was initiated in seven patients with double ventricular extrastimuli delivered during sinus rhythm or ventricular pacing and in three patients with double ventricular extrastimuli delivered during ventricular tachycardia. Four patients had spontaneous conversion to sinus rhythm and the remainder underwent defibrillation without sequelae. Recurrent ventricular fibrillation occurred clinically in 7 of the 10 patients. This study suggests that ventricular fibrillation occurs uncommonly during programmed ventricular stimulation and only in response to double ventricular extrastimuli in patients in whom spontaneous episodes are likely to occur.

Adolescent↗
PubMed1975

Recurrent ventricular fibrillation and modes of death in survivors of out-of-hospital ventricular fibrillation.

We examined the causes of death in patients previously resuscitated from out-of-hospital ventricular fibrillation. In 51 months, 234 patients were sucessfully resuscitated, hospitalized and discharged home. During follow-up observation, 89 episodes of recurrent ventricular fibrillation or death (or both) occurred, 64 of which (72 per cent) were unexpected, out-of-hospital circulatory arrests. Ventricular fibrillation occurred in 77 per cent of the 44 episodes in which the electrocardiogram was observed. Ten patients survived one or more episodes of recurrent ventricular fibrillation. Median time to recurrent ciruclatory arrest was 20 weeks after the preceding episode. Prodromal symptoms were infrequent, and activity levels were generally low at the time of cardiac arrest. Recurrent ventricular fibrillation of sudden death (or both) occurred predominantly when the initial episode was not associated with acute myocardial infarction. Patients resuscitated from ventricular fibrillation are susceptible to early recurrence, probably reflecting continuing myocardial electrical instability.

Adult↗
PubMed1975

[Ventricular fibrillation in acute phase of myocardial infarct. 1. Relationship between the development of ventricular fibrillation in myocardial infarct and previous rhythm disorders].

The author analyses the results of experimental studies in dogs and cats, that included a continuous recording of ECG, electrogram and monophase cardiac potentials during 1 hour following coronary artery ligation. The ligation caused bradycardia, but no correlation was found between the degree of bradycardia and the development of extrasystole and ventricular fibrillation. Extrasystole developed in 100% of the experiments in which the coronary artery ligation resulted in ventricular fibrillation, and in 66% and 87% of those without this complication, conducted in dogs and cats respectively. The rate of extrasystole proved important for the prognosis of fibrillation. The number of extrasystoli noted during the mean time of the development of fibrillation was 5 times higher in the experiments with ventricular fibrillation than in those without fibrillation. In the experiments with fibrillation the extrasystoli tended to occur earlier within the cardiac cycle. Of the total number of extrasystoli, grouped extrasystoli comprised 89% in the experiments with ventricular fibrillation, and 21%--in those without fibrillation. Ventricular tachystystole was noted in 50% of the experiments with fibrillation and in 17% of those without this complication. In the experiments complicated by fibrillation the period of ventricular tachysystole was characterized by a gradual shortening of the cardiac cycles.

Acute Disease↗
PubMed1978

Contrast agents lower ventricular fibrillation threshold.

Ventricular fibrillation thresholds were measured in anesthetized, closed-chest dogs during the injection of Renografin 76 or Conray 400 into the left coronary artery. Both agents significantly lowered fibrillation threshold--Renografin to 58 +/- 7%; Conray to 20 +/- 5% of control, respectively. The experimental method estimates fibrillatory potential of contrast media more precisely than previous methods. The initial results parallel relative toxicities observed in clinical usage.

Animals↗
PubMed1975

Ventricular fibrillation without left ventricular venting. Observations in humans.

Pressures were measured in the heart and great vessels of 52 patients who underwent coronary revascularization. In 25 patients the left ventricle was vented during fibrillation; in the others a vent was not used. Samples for blood gas analysis were obtained twice during fibrillation from the aorta, left atrium, pulmonary artery, and right atrium. Left ventricular venting was found to be effective in keeping mean left heart pressure below 10 mm Hg, although temporary incompetence of the aortic valve or malfunction of the vent occasionally caused higher pressures. Vent use led to air embolism in the aorta in 16% of the patients. In the nonvented patients mean left heart pressures remained between 10 and 20 mm Hg. However, higher values were frequently observed. Blood gas analysis demonstrated that without venting, retrograde pulmonary flow occurred during fibrillation. No abnormality was encountered that could be related to nonventing.

Aorta↗
PubMed1975

Electrophysiological mechanisms involved in ventricular fibrillation.

This report reviews the electrophysiological mechanisms involved in the initiation, maintenance, and termination of ventricular fibrillation. Ventricular fibrillation may be defined as chaotic, random, asynchronous electrical activity of the ventricles due to repetitive re-entrant excitation and/or rapid focal discharge. The capacity to fibrillate is inherent in ventricular muscle because the electrophysiological properties of the various segments of the ventricle are not uniform. Factors that enhance electrical asynchrony facilitate, while factors that decrease electrical asynchrony hinder, the development of fibrillation. Ventricular fibrillation may result following stimulation during the vulnerable period; under certain circumstances, rapid ventricular rates produced by ventricular or supraventricular arrhythmias may provoke ventricular fibrillation. Once fibrillation is initiated, a large mass, brief refractory period, and slow conduction velocity favor perpetuation. Reducing the excitable ventricular mass to a value less than the amount necessary to support spontaneous fibrillation causes fibrillation to terminate. Depolarization of every cell in both ventricles is not necessary to terminate ventricular fibrillation in the entire heart.

Action Potentials↗
PubMed1976

[Ventricular fibrillation and asystole precursors in myocardial infarct].

Ventricular fibrillation and asystole are a frequent cause of death in myocardial infarction. The data of continuous monitoring the heart in 134 patients with acute myocardial infarction and ventricular fibrillation and asystole. The immediate precursors of ventricular fibrillation were predominantly ventricular extrasystoles. A frequent precursor of ventricular fibrillation consists in paroxysmal ventricular tachycardia. In some patients the ventricular fibrillation was preceded by the block of the bundle of His, non-paroxysmal ventricular tathycardia, escaping contractions and some other arrhythmias. A factor providing for the development of ventricular fibrillation consists in the Q-T interval lengthening on ECG. Ventricular asystole is usually preceeded by atrioventricular block, Stage II-III, and the block of the bundle of His, as well as by ventricular tachycardia and extrasystole, in some cases--by sinus bradycardia and sinoauricular block (weakness of the sinus node). The examination of the rhythm and conductivity disorders preceeding the ventricular fibrillation is of great importance in view of the possibilities of prevention of "arrhythmic death".

Acute Disease↗
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↗
PubMed1978

[Prevention of ventricular fibrillation in animal experiments].

The precursors of ventricular fibrillation and asystole developing after ligation of a branch of the coronary artery and adrenalin injection were studied in 30 albino rats. The comparative efficacy of antiarrhythmic agents (ajmalin, lidocaine, isoptin, visken) in the prevention of ventricular fibrillation induced by electric current was determined in 40 rats. Ventricular extrasystole and tachysystole as well as the block of the bundle of His branch were the most common precursors of ventricular fibrillation. In some experiments fibrillation was preceded by complete atrioventricular block, cardiac fibrillation, sinus bradycardia, nonparoxysmal ventricular tachycardia, and excaped ventricular contractions. Ventricular asystole was most frequently preceded by complete atrioventricular block and the bundle of His branch block. Among the antiarrhythmic agents studied, ajmalin proved most effective in prevention of ventricular fibrillation; it raised the fibrillation threshold in all animals. Lidocaine, which produced a prophylactic effect in 50% of experiments, was second in effectiveness. Changes in the ventricular fibrillation threshold due to the effect of these agents were statistically significant on the average. Isoptin and visken proved to be less effective.

Ajmaline↗
PubMed1992

Frequency analysis of ventricular fibrillation and resuscitation success.

In 56 patients, frequency analysis of the electrocardiogram of ventricular fibrillation exhibited power spectra with a distinct dominant frequency. The greatest success for resuscitation from ventricular fibrillation is recorded when ventricular fibrillation develops after the patient comes under coronary care. Of the 41 patients in whom the onset and first 8 s of ventricular fibrillation were artefact-free the mean dominant frequency of primary ventricular fibrillation (no cardiogenic shock or cardiac failure) in 21 patients was 6.2 +/- 0.2 Hz, significantly higher than the mean dominant frequency of the first 8 s of secondary ventricular fibrillation (cardiogenic shock or heart failure) (4.0 +/- 0.2 Hz, 20 patients, p = 0.0001). In these patients the peak-to-trough amplitude (ECG) of the first 8 s of ventricular fibrillation was similar in both primary and secondary ventricular fibrillation as was the mean duration of ventricular fibrillation prior to the first DC shock. There was a significantly lower success rate for resuscitation from secondary ventricular fibrillation (6 of 20 patients) compared with resuscitation from primary ventricular fibrillation (18 of 21 patients, chi 2 17.8, p = 0.001). Of the remaining 15 patients who were collapsed between 3 and 20 min before the arrival of the mobile coronary care unit, the dominant frequency of the first 8 s of ventricular fibrillation fell with increased duration of collapse (from 5.5 Hz at 3 min to a mean of 2.1 Hz at 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1975

[Recurrent ventricular fibrillation (author's transl)].

106 episodes of ventricular fibrillation were observed in 11 patients, 9 of whom had acute myocardial infarctions. The heart rate before the onset of ventricular fibrillation was below 50 in two episodes, 60 to 100 in 63, and above 100 in 41. 83 attacks of ventricular fibrillation were preceded by fewer than five ventricular premature beats, 23 by more than five, 19 by more than ten. Multifocal ventricular premature beats occurred ten times, runs of ventricular premature beats 11 times, with only three falling into the vulnerable period. Left bundle branch block was present in three patients, right bundle branch block with left anterior hemiblock in two, isolated left anterior hemiblock in two, left posterior hemiblock in one. 85 episodes of ventricular fibrillation occurred during antiarrhythmic treatment, 72 during lidocaine administration. Antiarrhythmic drugs were effective only in reducing the number of ventricular premature beats. The only successful treatment of recurrent episodes of ventricular fibrillation was repeated electrical countershocks.

Aged↗
PubMed1977

The effects of heart rate, myocardial ischemia and vagal stimulation on the threshold for ventricular fibrillation.

The minimum current required to cause ventricular fibrillation was determined by electrical stimulation of the normal or ischemic canine left ventricle. The threshold for ventricular fibrillation in the normal heart decreased when the heart rate was rapid. Strong vagal stimulation did not affect the ventricular fibrillation threshold when the heart rate was fixed. The fall in the ventricular fibrillation threshold in the presence of acute myocardial ischemia was greater and more prolonged when the heart rate was rapid. These findings indicate the importance of the immediate correction of tachycardia in patients suffering from acute myocardial infarction.

Animals↗
PubMed1976

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Arrhythmias, Cardiac↗
PubMed1976

Effect of nitroglycerin on ventricular fibrillation threshold of nonischemic myocardium.

The threshold for ventricular fibrillation induced by a 200 msec train of pulses was measured during a control period and during an intravenous infusion of nitroglycerin in 14 nonischemic open chest dogs. Infusion of nitroglycerin in doses sufficient to reduce mean arterial blood pressure an average of 17 mm Hg was associated with a rise in ventricular fibrillation threshold from a control value of 24 +/- 3 (mean +/- 1 standard error of the mean) to 41 +/- 6 milliamperes (P less than 0.001). In a subgroup of six animals simultaneous infusions of nitroglycerin and phenylephrine abolished the hypotensive effect of nitroglycerin but did not significantly alter the rise in ventricular fibrillation threshold observed with nitroglycerin infusion alone. In five other animals mean arterial blood pressure was similarly reduced an average of 17 mm Hg by venous hemorrhage, but was associated with a lowering than a rise in ventricular fibrillation threshold from a prehemorrhage value of 28 +/- 6 to 15 +/- 2 milliamperes, (P less than 0.005). Thus, intravenously administered nitroglycerin raises ventricular fibrillation threshold in nonischemic canine myocardium independent of its hypotensive effects.

Action Potentials↗