Detection of asystole, ventricular fibrillation and ventricular tachycardia with automated ECG monitoring.
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Arrhythmias, Cardiac↗
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[Recurrent attacks of ventricular fibrillation and ventricular tachycardia during myocardial infarct, treated successfully by defibrillation and indirect heart massage].
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Electric Countershock↗
[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↗
[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↗
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↗
[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↗
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↗
Repetitive extrasystole as an index of vulnerability to ventricular fibrillation.
The assessment of ventricular vulnerability by inducing ventricular fibrillation (VF) presents limitations when neural activity is being investigated, especially in the unanesthetized animal. As repetitive extrasystoles (RE) have been observed to precede the occurrence of VF, it was relevant to determine whether the RE threshold provides a reliable index of cardiac susceptivility to fibrillation. The RE and VF threshold relationships were studied in 32 chloralose-anesthetized dogs during left stellate ganglion stimulation, vagus nerve stimulation, and beta-adrenergic blockage with practolol. The vulnerable period was scanned at 1-ms intervals and at 2-mA increments with a single, 2-ms, constant-current cathodal stimulus; RE and multiple RE were induced reproducibly when 66% and 82%, respectively, of the fibrillatory current was administered. The nadirs for RE and multiple RE were coincident in the cardiac cycle with the vulnerable-period threshold for VF. Stellate and vagal stimulation and beta-adrenergic blockade resulted in comparable changes in RE and VF thresholds and produced equivalent shifts in the cardiac cycle of the RE and VF vulnerable-period nadirs. These observations suggest that RE and VF phenomena share a common electrophysiologic basis and that the RE threshold can be used as an end point for measuring ventricular vulnerability to VF.
Animals↗
Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion.
The effect of nitroglycerin on vulnerability to ventricular fibrillation was examined in 44 chloralose-anesthetized dogs. In 19 animals ventricular fibrillation threshold was measured before and during a 10 minute period of occlusion of the left anterior descending coronary artery followed by abrupt release of occlusion. Fibrillation threshold was determined using the single stimulus and train of stimuli methods. The influence of nitroglycerin on vulnerability was assessed with and without prevention of the drug's hypotensive effect by intravenous injection of phenylephrine. In the nonischemic myocardium, infusion of nitroglycerin alone or in combination with phenylephrine did not alter the ventricular fibrillation threshold. However, during both coronary occlusion and reperfusion, administration of nitroglycerin alone afforded partial protection against vulnerability to ventricular fibrillation. Nearly complete protection was imparted by combined administration of nitroglycerin and phenylephrine. The incidence of spontaneous ventricular fibrillation during reperfusion was significantly reduced by combined administration of nitroglycerin and phenylephrine. It is concluded that infusion of nitroglycerin decreases susceptibility to ventricular fibrillation during both acute myocardial ischemia and reperfusion and that this beneficial action is substantially enhanced when the drug's hypotensive effect is prevented.
Animals↗
Cyclic AMP as a determinant of vulnerability to ventricular fibrillation in the isolated rat heart.
Ventricular fibrillation threshold and vulnerable period were measured in the isolated perfused rat heart to assess the influence of dibutyryl cyclic AMP on ventricular vulnerability. Doses of dibutyryl cyclic AMP of 0.6-1.6 mumol/min caused an increase in coronary flow but had no effect on vulnerability, whereas doses of 2.6-4.2 mumol/min resulted in an increase in coronary flow, a decrease in VF threshold, and an increase in the width of the vulnerable period. These experiments support the concept of a local myocardial action of catecholamines, mediated by cyclic AMP, whereby vulnerability to ventricular fibrillation is increased.
Animals↗
Ventricular fibrillation in the Wolff-Parkinson-White syndrome.
To examine the risk of ventricular fibrillation in patients with the Wolff-Parkinson-White syndrome, we compared patients who had this syndrome and a history of ventricular fibrillation related to preexcitation with patients who had the syndrome without this history. Ventricular fibrillation occurred during atrial fibrillation, with rapid conduction over the accessory pathway, and these patients had a higher prevalence of both reciprocating tachycardia and atrial fibrillation (14 of 25 vs. 18 of 73, P = 0.004) and multiple accessory pathways (five of 25 vs. four of 73, P = 0.012). The shortest preexcitation R-R interval during atrial fibrillation was less in the group with ventricular fibrillation (mean shortest R-R, 180 vs. 240 milliseconds, P less than 0.0001) as was the average R-R interval (mean average R-R, 269 vs 340 milliseconds, P less than 0.0001). Patients with Wolff-Parkinson-White syndrome who are most susceptible to ventricular fibrillation have a history of atrial fibrillation and reciprocating tachycardia, demonstrate rapid conduction over an accessory pathway during atrial fibrillation and have multiple accessory pathways.
Adolescent↗
Risk-benefit stratification as a guide to lidocaine prophylaxis of primary ventricular fibrillation in acute myocardial infarction: an analytic review.
Early investigators suggested that ventricular fibrillation without heart failure in acute myocardial infarction was reliably preceded by warning arrhythmias, and that suppression of such arrhythmias with intravenous lidocaine could avoid the need for resuscitation. While the efficacy and safety of lidocaine have been substantiated, the reliability of warning arrhythmias as predictors for primary ventricular fibrillation has not. We present data showing that the risk of primary ventricular fibrillation is most dependent on the patient's age and the interval since the onset of his symptoms, rather than on the presence of warning arrhythmias. We have estimated that lidocaine prophylaxis would have to be given to about 12 patients in the highest risk group (patients under age 50 and within six hours of the onset of symptoms), compared to about 400 patients in the lowest risk group (patients above age 70 and more than 24 hours since the onset of symptoms), to prevent one episode of primary ventricular fibrillation in each group. We propose that these risk stratifications, as adapted to the conditions in specific hospitals, provide the most rational approach to lidocaine prophylaxis of primary ventricular fibrillation.
Age Factors↗
Dibenzepin as an antifibrillatory agent for spontaneously terminating electrically induced ventricular fibrillation.
The effect of dibenzepin, a tricyclic antidepressant drug, on electrically induced ventricular fibrillation was studied in 20 cats and nine dogs. The ventricular fibrillation threshold and the ability of the ventricle to defibrillate spontaneously were determined before and after the administration of dibenzepin, with each animal serving as its own control. The drug raised the ventricular fibrillation threshold in all the animals tested. Before treatment, spontaneous ventricular defibrillation occurred in only 8 of the 20 cats and in none of the dogs. After treatment, all of the cats and eight of the dogs exhibited spontaneous ventricular defibrillation. The study of drugs that have a self-defibrillatory effect may serve to further understanding of the mechanism of ventricular fibrillation and its spontaneous termination.
Animals↗
Effects of ventricular fibrillation on coronary blood flow and myocardial metabolism.
Ventricular fibrillation is frequently induced during cardiac surgery to quiet the operative field. The reported effects of fibrillation on the myocardium vary considerably. In an attempt to better define these effects, we subjected 28 dogs to one hour of total normothermic bypass. Myocardial blood flow, lactate, adenosine triphosphate (ATP), oxygen consumption, and left ventricular fibrillation was induced in 5 dogs and continuous electrical fibrillation in 7 dogs. These groups were compared to two respective control groups with beating hearts of 8 animals each. Coronary sinus flow, total coronary blood flow, left ventricular flow, myocardial oxygen consumption, and myocardial tissue lactate increased significantly in the fibrillating hearts. Left ventricular dp/dt decreased with fibrillation, but not significantly. It is concluded that the metabolic demands of ventricular fibrillation exceed the increase in coronary blood flow, when compared to demands of the beating heart, and that decreased left ventricular performance may result.
Adenosine Triphosphate↗
Repolarization abnormalities in survivors of out-of-hospital ventricular fibrillation.
Survivors of out-of-hospital ventricular fibrillation (VF) are at high risk for recurrent VF, probably reflecting continued myocardial electrical instability. In this study 12-lead ECGs of 125 VF survivors with coronary heart disease were examined and compared to those of 98 ambulatory post-MI patients. The study was part of an effort to define clinical identifiers of patients likely to develop sudden cardiac death. Ventricular fibrillation survivors were commonly had premature ventricular complexes (PVCs):30% versus 13% (P less than 0.01). In addition, ECGs of VF survivors showed a significantly greater prevalence of ST-segment depression (46% versus 10%), T wave flattening (52% versus 26%), and QTc prolongation (35% versus 18%). It is proposed that these repolarization abnormalities represent asynchronous repolarization, which together with frequent PVCs, may set the stage for re-entrant ventricular dysrhythmias and ultimately VF. It is also possible that repolarization abnormalities together with premature ventricular contractions might serve as markers of patients with coronary heart disease who are at increased risk for sudden cardiac death.
Aged↗
Cardia lymph in electrical ventricular fibrillation: an experimental study.
The flow velocity of cardiac lymph during electrical ventricular fibrillation under normothermic cardiopulmonary bypass was studied experimentally in dogs. The time needed for the cardiac lymph node to become stained after injection of dye into the apex myocardium of the left ventricle was measured as an indicator in determining flow velocity of cardiac lymph. The flow velocity was markedly decelerated immediately after the commencement of electrical ventricular fibrillation. It was accelerated, however, after 2 hours of continuous electrical ventricular fibrillation. The difference between the two values was significant (p less than 0.01). Absent contractility of the heart influenced the deceleration of flow velocity of cardiac lymph immediately after the commencement of electrical ventricular fibrillation. Acceleration after 2 hours involved stasis of cardiac lymph as a result of absent contractility and increment of lymph production due to the nonphysiological condition of the myocardium.
Animals↗
Disopyramide-induced ventricular fibrillation.
Three cases are described with documented ventricular fibrillation shortly after the patients received disopyramide in moderate dosage. Electrocardiograms showed markedly prolonged Q-T intervals in two patients and a prominent U wave with a prolonged Q-U interval in one patient, but no change in QRS width. Disopyramide-induced ventricular fibrillation appears to be similar to that caused by quinidine and is an indication to discontinue the drug.
Administration, Oral↗
The effects of coronary artery disease on the ventricular fibrillation threshold in man.
The ventricular fibrillation threshold (VFT) was measured in 28 patients at the time of cardiac surgery. The VFT was measured with a 100 Hz train of 24 rectangular pulses positioned across the ST segment and T wave. Current was applied to the epicardial surface of either ventricle with a bipolar electrode probe. In six patients, the normal right VFT was 24.3 +/- 5.2 mA, and in 10 patients the normal left VFT was 33.6 +/- mA (p less than 0.05). In 12 patients with greater than or equal to 75% obstruction of the left anterior descending coronary artery, the left VFT was 18.6 +/- 6.9 mA. This value was significantly less than the left VFT in patients without coronary artery disease (p less than 0.001). This study shows that the VFT can be measured in man and that coronary artery disease reduces this parameter.
Adult↗