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PubMed1988

Fourier analysis of ventricular fibrillation and synchronization of DC countershocks in defibrillation.

Spectral analysis of the first 40 seconds of ventricular fibrillation confirmed the presence of a large periodic component in fibrillation, with a dominant frequency of 9.9 +/- 0.7 Hz and a narrow bandwidth. To determine whether less energy was required for defibrillation at any particular phase of the ventricular fibrillation cycle, the authors studied the effect of synchronization of the countershock to the peaks and troughs of the ventricular fibrillation waveform in 12 dogs anesthetized with sodium pentobarbitone (35 mg/kg iv). There was no significant difference in threshold-delivered energy or threshold-delivered current between shocks synchronized to the peaks of ventricular fibrillation, shocks synchronized to the troughs of ventricular fibrillation, and unsynchronized shocks.

Animals↗

PubMed1984

Pre- and in-hospital antiarrhythmic prevention of ventricular fibrillation complicating acute myocardial infarction.

Prehospital prevention of primary ventricular fibrillation using 300 mg lidocaine intramuscularly seems to be ineffective in view of the rather low plasma lidocaine levels obtained with this regimen. Preliminary results of 400 mg lidocaine administered by paramedics using an automatic injector are encouraging. In-hospital prevention of primary ventricular fibrillation can be achieved by routine administration of intravenous lidocaine in rather high dosages provided that adequate measures are taken. When, however, recurrent attacks of primary ventricular fibrillation supervene, repeated defibrillation seems to be preferable rather than continuous institution of various antiarrhythmic drugs.

Aged↗

PubMed1979

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↗

PubMed1977

Prevention of ventricular fibrillation in experimental myocardial infarction.

The fall in the ventricular fibrillation threshold during the first half an hour following ligation of the descending branch of the left coronary artery in dog was not influenced by the i.v. injection of trimecain (Mesokain Spofa). On the other hand, an i.v. injection of methypranol (Trimepranol Spofa) given prior to ligation increased the level of ventricular fibrillation threshold 3 to 4 times compared to control value before occlusion in all 10 studied dogs. Depression of the beta-blocking adrenergic activity may thus prevent the occurrence of ventricular fibrillation in acute myocardial ischaemia.

Animals↗

PubMed1999

Increase in heart rate precedes episodes of ventricular tachycardia and ventricular fibrillation in patients with implantable cardioverter defibrillators: analysis of spontaneous ventricular tachycardia database.

Patients with heart disease and decreased heart rate variability (HRV) have an increased risk of all-cause mortality as well as arrhythmic death. The question of acute changes in HRV immediately preceding arrhythmic events remains unanswered. We analyzed data from patients with implantable cardioverter defibrillators who had ventricular tachycardia (VT) or ventricular fibrillation (VF) detected by the device. The device stores 1,000 consecutive RR intervals preceding the arrhythmic event detection and before device interrogation. Compared to this control segment, the mean heart rate (HR) increased prior to the arrhythmic event for both VT (88.5 vs 72.7 beats/min, P < 0.0005) and VF (85.4 vs 73.3 beats/min, P < 0.05) patients. No difference in HRV (as analyzed by a time-domain, frequency-domain [fast Fourier transform], and a nonlinear technique) has been detected. We estimated the amount of ectopic beats from the number of RR intervals that differed from the preceding RR interval by > 10%. The frequency of such beats was significantly higher in the prearrhythmic data segments than in the control segments for VT (10.7 vs 6.6/50 beats, P < 0.05) although not for VF (9.8 vs 6.1/50 beats, NS). We conclude that the HR and frequency of ectopic beats are higher prior to onset of the arrhythmic events, although HRV does not change markedly. These results are consistent with sympathetic activation being the predominant autonomic change prior to VT/VF onset in this patient population.

Adult↗

PubMed1989

Cell calcium in the pathophysiology of ventricular fibrillation and in the pathogenesis of postarrhythmic contractile dysfunction.

The mechanism of ventricular fibrillation is poorly understood at the cellular level. We explored the role of intracellular free calcium in the pathophysiology and pathogenesis of ventricular fibrillation in perfused ferret hearts loaded with the Ca2+ indicator 5F-BAPTA. Nuclear magnetic resonance spectroscopy was used to measure [Ca2+]i, pH, and high-energy phosphates. During ventricular fibrillation induced by burst pacing, [Ca2+]i rose rapidly and dramatically, exceeding by four times the control within 5 minutes. [Ca2+]i remained markedly elevated throughout 20 minutes of fibrillation, but it returned to control values shortly after defibrillation. In a group of hearts kept isovolumic by a balloon in the left ventricle, acidosis and high-energy phosphate depletion developed despite the maintenance of normal coronary pressure. To distinguish the effects of superimposed ischemia from those of the arrhythmia itself, we lowered left ventricular volume during fibrillation in a second group of hearts. This maneuver decreased wall stress such that fibrillation had no significant adverse effect on intracellular pH, high-energy phosphates, or lactate efflux. [Ca2+]i still increased remarkably despite the absence of ischemic changes. Developed pressure did not recover to control levels after defibrillation in either group; the hearts appeared "stunned." We conclude that intracellular calcium increases as a direct consequence of ventricular fibrillation. The increase in [Ca2+]i may cause the contractile dysfunction observed in postarrhythmic hearts. Its possible role in initiating or maintaining the arrhythmia is less clear.

Animals↗

PubMed1989

Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation.

The clinical efficacy of intravenous amiodarone in terminating sustained ventricular tachycardia and in preventing recurrences of ventricular tachycardia and ventricular fibrillation was evaluated in 26 patients. All of them presented with organic heart disease accompanied by depressed left ventricular function. Intravenous amiodarone terminated spontaneous ventricular tachycardia in eight of 19 patients. Fifteen of the 26 patients had had at least one episode of ventricular tachycardia or ventricular fibrillation each day in the period immediately before the intravenous administration of amiodarone. Amiodarone controlled ventricular tachycardia or ventricular fibrillation in nine of these 15 patients; in three further cases it was successful when supplemented by additional administration of a previously ineffective antiarrhythmic drug and ventricular pacing. Two patients died despite these measures. In one, the amiodarone infusion had to be stopped because of an arrhythmogenic effect. Sustained deterioration of haemodynamic function or of pre-existing intraventricular conduction disturbances was never seen. Intravenous amiodarone was effective in terminating sustained ventricular tachycardia and in preventing frequent episodes of ventricular arrhythmia that were refractory to other antiarrhythmic drugs.

Amiodarone↗

PubMedDate not supplied

Transesophageal echocardiographic evaluation of the morphologic and hemodynamic cardiac changes during ventricular fibrillation.

To analyze cardiac motion during ventricular fibrillation (VF), we used transesophageal echocardiography to study nine male subjects, aged 44 +/- 7 years, affected by heart disease who have poor left ventricular function, during implantation of an Implantable Cardioverter Defibrillator, when VF is induced several times to determine the defibrillation threshold. Wall and valvular motion, transmitral and transaortic blood flow, and blood echoreflectivity were evaluated in all patients. Moreover, in basal conditions, during VF, 1 and 5 minutes after restoration of basal rhythm, we calculated the left ventricular end-diastolic volume (EDLVV) and area (EDLVA), the left ventricular end-systolic volume and area, the ejection fraction, and the fractional area change with a four-chamber echocardiographic view. At the onset of VF, the myocardium and valves exhibited a chaotic motion. About 10 seconds later the oscillatory movement of the heart walls became more ample and regular; the mitral valve showed a cyclic closure and opening with a forward flow, and the aortic valve exhibited similar behavior, although at a lower intensity. A spontaneous echo contrast appeared inside the atrial and ventricular cavities, gradually becoming an incrt homogeneous mass that was completely flushed away with the restoration of the basal rhythm. When VF started, EDLVV (286 +/- 98 ml) and EDLVA (50 +/- 16.5 cm2) decreased abruptly (EDLVV = 182 +/- 65 ml, p < 0.02; EDLVA = 38 +/- 9.2 cm2,p < 0.05); so did ejection fraction (31.8% +/- 15% versus 11% +/- 5%; p < 0.003) and fractional area change (25.8% +/- 6.5% versus 7% +/- 3.4%; p < 0.001). When the basal rhythm was restored, the heart extended again and EDLVV, EDLVA, ejection fraction, and fractional area change after 1 and 5 minutes were similar to those calculated before induction of VF. This behavior was observed during both the first and last induced VF. Thus during VF, great variations of heart morphology and dynamics, as well as blood echoreflectivity, occur; the heart seems to make attempts to organize its dynamics during the arrhythmia. Repeated episodes of VF and defibrillation with low energies do not seem to worsen left ventricular dynamics even in impaired hearts.

Adult↗

PubMed2006

Altered electrical activity of fibrillation process following thrombolytic therapy in out-of-hospital cardiac arrest patients with sustained ventricular fibrillation.

The likelihood of successful defibrillation in patients with sustained ventricular fibrillation (VF) is increased after administering thrombolytics during cardiopulmonary resuscitation (CPR). While dissolution of coronary artery thrombosis resolves the underlying cause of myocardial infarction in the majority of patients, improved microcirculatory reperfusion and alteration of the electrical activity of the fibrillation process may increase the likelihood of restoring spontaneous circulation in cardiac arrest patients. Electrocardiography is a sensitive means of displaying current myocardial perfusion in VF using changes in the frequency and amplitude of fibrillation. Our hypothesis postulates that thrombolytic therapy during CPR increases fibrillation frequency, fibrillation amplitude and amplitude spectrum area, thus improving ventricular fibrillation status and the chance of successful defibrillation.

Cardiopulmonary Resuscitation↗

PubMed1992

A fast Fourier transform analysis of coronary reperfusion-induced ventricular fibrillation and the modification by dibutyryl cyclic AMP in a cat model.

To investigate the effect of dibutyryl cyclic AMP (dbcAMP) on ventricular fibrillation after coronary reperfusion, the proximal portion of the anterior descending branch of left coronary artery was reperfused 20 min after ligation in 24 cats. McFee X Y Z electrocardiograms were recorded and ventricular fibrillation was analyzed using a fast Fourier transform analysis (FFT). Ventricular fibrillation occurred in 20 of 24 cases. Sixty seconds after the occurrence of ventricular fibrillation, an intracardiac infusion of dbcAMP was administered. Nine of the 20 were defibrillated and converted to sinus rhythm or junctional rhythm after the administration of dbcAMP. The amplitude and frequency of the main power spectrum of the ventricular fibrillation waves were analyzed by FFT before and after the infusion of saline or dbcAMP. In the saline group there was no significant change in FFT. However, in the dbcAMP group, the amplitude increased significantly from 0.036 +/- 0.015 (MV--2) to 0.054 +/- 0.013 (MV--2) (p < 0.01) and the frequency decreased significantly from 4.22 +/- 1.37 (Hz) to 1.33 +/- 0.91 (Hz) (p < 0.01). Those results indicate that dbcAMP increased the amplitude and decreased the frequency of the main power spectrum of ventricular fibrillation analyzed by FFT. These distinctive changes in FFT analysis were associated with defibrillation in 9 of 20 cases.

Animals↗

PubMed1998

Detection of ventricular fibrillation by transvenous defibrillating leads: integrated versus dedicated bipolar sensing.

INTRODUCTION: Dedicated bipolar sensing has been suggested to be safer than integrated bipolar sensing due to an increased incidence of failure to redetect ventricular fibrillation after an unsuccessful shock with leads that use integrated bipolar sensing. We compared sensing characteristics during ventricular fibrillation of simultaneously recorded dedicated and integrated bipolar electrograms. METHODS AND RESULTS: Thirty patients undergoing transvenous defibrillator implantation with a Transvene lead were studied. Simultaneous recordings were made from the dedicated bipole and the integrated bipole from the distal tip to the coil (interelectrode distance 18.3 mm). The mean detection time and number of undetected beats for the initial episode of ventricular fibrillation were 2804 +/- 569 msec and 0.9 +/- 0.8 using the dedicated recordings and 2938 +/- 546 msec and 1.4 +/- 1.1 (P = 0.026) using the integrated recordings. The mean redetection times and number of undetected beats following a failed first shock (n = 13) were 2468 +/- 225 msec and 0.8 +/- 1.1 for the dedicated recordings and 3042 +/- 498 msec (P < 0.0003) and 4.2 +/- 4.2 (P < 0.005) for the integrated recordings. Frequency analysis of the ventricular fibrillation electrograms demonstrated that the signal energy in the dedicated electrograms was significantly greater than the energy in the integrated electrograms (P < 0.0001). There was a significant negative relationship between detection times and the ventricular fibrillation signal energy. There was no independent effect of recording type (dedicated versus integrated). CONCLUSION: There are only minor differences in detection/redetection of ventricular fibrillation between dedicated and integrated (with tip to coil spacing of 18.3 mm) recording configurations. Detection times during ventricular fibrillation are related to the signal variance or energy recorded. Differences in the sensing performance of the two recording configurations can be explained by the differences in signal energy between the dedicated and integrated recordings that occur during ventricular fibrillation.

Defibrillators, Implantable↗

PubMed2004

Effects of cardiopulmonary resuscitation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest.

BACKGROUND: Early defibrillation is considered the most important factor for restoring spontaneous circulation in cardiac arrest patients with ventricular fibrillation. Recent studies have shown that, after prolonged ventricular fibrillation, the rates of return of spontaneous circulation (ROSC) and survival are improved if defibrillation is delayed so that CPR can be given first. To examine whether CPR improves myocardial readiness for defibrillation, we analyzed whether CPR causes changes in predictors of defibrillation success calculated from the ventricular fibrillation waveform. METHODS AND RESULTS: ECG recordings were retrieved for 105 patients from an original study of 200 patients receiving CPR or defibrillation first. Altogether, 267 CPR sequences from 77 patients were identified on which the effect of CPR could be evaluated. Five predictors of ROSC (spectral flatness measure, energy, centroid frequency, amplitude spectrum relationship, and estimated probability of ROSC) were determined from a spectral analysis of the ventricular fibrillation waveform immediately before and immediately after each of the 267 sequences. CPR increased spectral flatness measure, centroid frequency, and amplitude spectrum relationship (P<0.05, P<0.001, P<0.01). In an analysis of the effect of the duration of CPR, the probability of ROSC and amplitude spectrum relationship showed a positive change for CPR sequences lasting >3 minutes (P<0.001, P<0.05). CONCLUSIONS: During resuscitation from ventricular fibrillation, changes in the predictors calculated from the ventricular fibrillation waveform indicated a positive effect of CPR on the myocardium.

Cardiopulmonary Resuscitation↗

PubMed1996

Increased precordial QTc dispersion predicts ventricular fibrillation during acute myocardial infarction.

Electrocardiograms of 19 consecutive patients with acute myocardial infarction complicated by early ventricular fibrillation were compared with those in 19 case-matched patients with acute myocardial infarction not complicated by ventricular fibrillation. The mean precordial QTc interval dispersion in patients with ventricular fibrillation was greater than that of patients without ventricular fibrillation (73 +/- 28 ms vs 30 +/- 12 ms, p < 0.001).

Electrocardiography↗

PubMed1986

The effect of chemical ablation of the endocardium on ventricular fibrillation threshold.

The purpose of this study was to examine the effects of ablation of the superficial endocardium and Purkinje network on left ventricular fibrillation threshold. Lugol's solution was applied through small ventriculotomies to the left and right ventricular endocardium of 10 dogs on cardiopulmonary bypass. Two control groups of five animals each underwent either endocardial application of saline or epicardial application of Lugol's solution. Ventricular fibrillation threshold was measured before and after each intervention by the single-stimulus technique. Application of Lugol's solution to the endocardium resulted in a 102 +/- 15% increase in ventricular fibrillation threshold from a control value of 26 +/- 2 to 53 +/- 6 mA (p less than .005). In two animals, ventricular fibrillation could not be initiated postoperatively. In the control groups, there were no significant changes in ventricular fibrillation threshold. Histologic examination revealed that Lugol's solution obliterated less than 0.5 mm of superficial endocardium while sparing the adjacent myocardium. Electrophysiologic and rheologic data confirmed the discrete nature of the chemical injury. Thus ablation of the superficial ventricular endocardium with Lugol's solution results in a profound increase in the ventricular fibrillation threshold with only minimal tissue destruction.

Animals↗

PubMed1995

[Reduction of incidence of ischemia-reperfusion induced ventricular fibrillation by captopril].

To investigate the role of catecholamine and prostacyclin in ischemia reperfusion-induced ventricular fibrillation, experiments were performed in rat hearts using methods of radioimmunoassay and fluorohistochemistry. Regional myocardial ischemia was induced by ligation of the left coronary artery followed by reperfusion. In the ischemia reperfusion group, ventricular fibrillation during reperfusion took place in 78% of the hearts. In the group pretreated with captopril, the incidence of ventricular fibrillation decreased significantly (65.5%). In comparison with the ischemia reperfusion group, myocardial catecholamine content and 6-keto-PGF1 alpha of the captopril group were significantly increased (P < 0.01) while thromboxane B2 (TxB2) and TxB2/6-keto-PGF1 alpha were decreased (P < 0.01). In Ang II group, infusion of angiotensin II reversed the protective effect of captopril and restored the incidence of ventricular fibrillation (85%), while myocardial catecholamine content was not different from the ischemia reperfusion group (P > 0.05). Above results suggest that reduction of the incidence of ischemia reperfusion-induced ventricular fibrillation by captopril may be due to its inhibition on angiotensin II production with consequent reduction of the release of myocardial catecholamine, suppression of TxB2 and promotion of PGI2 synthesis.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

Incidence of ventricular fibrillation after aortic cross-clamp release using lignocaine cardioplegia.

The occurrence of ventricular fibrillation after aortic de-clamping during cardiac surgery is common, and if prolonged may contribute to myocardial ischaemia. The use of lignocaine cardioplegia to minimize reperfusion ventricular fibrillation was studied in 141 patients undergoing first time coronary artery surgery in a double blind prospective randomized trial: 71 patients received lignocaine 100 mg/l in their cardioplegia, whereas a control group of 70 patients received cardioplegia without lignocaine. Lignocaine cardioplegia reduced significantly the incidence of reperfusion ventricular fibrillation from 63% to 42%. Of those patients developing reperfusion ventricular fibrillation, a higher proportion receiving lignocaine cardioplegia underwent spontaneous defibrillation (30% vs 11%) though this was not statistically significant. The incidence of atrio-ventricular (A-V) block necessitating ventricular pacing to separate from cardiopulmonary bypass was significantly higher in the lignocaine treated group (44%) than in the control group (20%): this may have been due to the additive effect of procaine in the cardioplegia solution. In the majority of cases this A-V block was transient and had resolved prior to the completion of surgery.

Adult↗

PubMed2002

Idiopathic ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome.

Ventricular fibrillation in a patient with ventricular preexcitation is usually due to atrial fibrillation with an extremely rapid ventricular rate from which it degenerates. We present a case with Wolff-Parkinson-White syndrome and coexistent idiopathic ventricular fibrillation. The patient, a 23-year-old male, had had a cardiac arrest four years earlier. In electrophysiological study, the accessory pathway was located in the left posteroseptal region and successfully eliminated with radiofrequency catheter ablation. After the ablation procedure, ventricular fibrillation was induced with programmed ventricular stimulation. A dual chamber implantable cardioverter defibrillator was implanted in the patient.

Adult↗

PubMed1987

Idiopathic ventricular fibrillation: inducibility and beneficial effects of class I antiarrhythmic agents.

Ventricular fibrillation in patients without recognizable heart disease is uncommon and electrophysiologic data on such patients is limited. Over a 7 year period, five patients (three men and two women, ranging in age from 24 to 52 years) without demonstrable heart disease underwent electrophysiologic studies with pharmacologic drug testing because of single (four patients) or multiple (one patient) documented episodes of ventricular fibrillation. The arrhythmic event was unrelated to myocardial ischemia or infarction, metabolic or electrolyte disturbances, drug toxicity, preexcitation, or prolonged QT syndromes. In all three patients receiving no antiarrhythmic drugs and in two pretreated with amiodarone, a rapid poorly tolerated ventricular tachyarrhythmia requiring cardioversion was induced by programmed ventricular stimulation with up to two extrastimuli. In all instances, addition of either oral quinidine or oral disopyramide prevented the induction of sustained ventricular arrhythmias. All five patients were placed on antiarrhythmic drug regimens found effective during electrophysiologic studies and remained asymptomatic during follow-up periods ranging from 12 to 93 (mean 52) months. We conclude that in the patients with idiopathic ventricular fibrillation in our study: programmed ventricular stimulation reliably replicated the spontaneous arrhythmia, class I antiarrhythmic agents effectively prevented induction of the arrhythmia in the laboratory, and in contrast to the severity of the presenting arrhythmia, a benign clinical course was observed during long-term therapy with class I antiarrhythmic agents.

Adult↗