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PubMed1997

Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation.

BACKGROUND: Studies in animals have suggested that intravenous vasopressin is associated with better vital-organ perfusion and resuscitation rates than is epinephrine in the treatment of cardiac arrest. We did a randomised comparison of vasopressin with epinephrine in patients with ventricular fibrillation in out-of-hospital cardiac arrest. METHODS: 40 patients in ventricular fibrillation resistant to electrical defibrillation were prospectively and randomly assigned epinephrine (1 mg intravenously; n = 20) or vasopressin (40 U intravenously; n = 20) as primary drug therapy for cardiac arrest. The endpoints of this double blind study were successful resuscitation (hospital admission), survival for 24 h, survival to hospital discharge and neurological outcome (Glasgow coma scale). Analyses were by intention to treat. FINDINGS: Seven (35%) patients in the epinephrine group and 14 (70%) in the vasopressin group survived to hospital admission (p = 0.06). At 24 h, four (20%) epinephrine-treated patients and 12 (60%) vasopressin-treated patients were alive (p = 0.02). Three (15%) patients in the epinephrine group and eight (40%) in the vasopressin group survived to hospital discharge (p = 0.16). Neurological outcomes were similar (mean Glasgow coma score at hospital discharge 10.7 [SE 3.8] vs 11.7 [1.6], p = 0.78). INTERPRETATION: In this preliminary study, a significantly larger proportion of patients created with vasopressin than of those treated with epinephrine were resuscitated successfully from out-of-hospital ventricular fibrillation and survived for 24 h. Based upon these findings, larger multicentre studies of vasopressin in the treatment of cardiac arrest are needed.

Aged↗

PubMed1983

Calcium antagonists, ventricular fibrillation, and enzyme release in ischemic rat hearts.

Early experiments with the calcium antagonist verapamil showed that it could inhibit the transsarcolemmal influx of calcium ions induced by isoproterenol in ventricular myocardium without inhibiting the effect of beta stimulation to increase tissue cyclic AMP. Current views of the effects of the beta-receptor-adenylate cyclase-cyclic AMP system of the calcium channel suggest that both calcium antagonists and beta-adrenoceptor antagonists should inhibit transsarcolemmal calcium influx if calcium is the third messenger of beta-agonist catecholamines. When high concentrations of circulating catecholamines are added to normal isolated hearts, two of the effects include increased vulnerability to ventricular fibrillation and high rates of enzyme release. These effects are antagonized by beta-adrenoceptor inhibitors and by calcium antagonists, which suggests a classical second (cyclic AMP) and third (calcium) messenger effect. In the presence of coronary artery ligation, the ventricular fibrillation threshold falls and enzyme release is enhanced. Both effects are associated with an increased tissue cyclic AMP level in the ischemic zone and are susceptible to calcium antagonist procedures. Neither effect can be fully stopped by beta-adrenoceptor antagonism. Therefore the evidence from this model with coronary artery ligation favors the views that 1) cyclic AMP accumulates in ischemic tissue by a process not fully susceptible to inhibition by beta-adrenoceptor antagonists; and 2) calcium ions are associated with the development of ventricular fibrillation and enzyme release by a process susceptible to inhibition by calcium antagonist agents such as verapamil, nifedipine, and diltiazem.

Adrenergic beta-Antagonists↗

PubMed1979

[Ventricular fibrilation in children: electrical treatment (author's transl)].

Experience on the treatment of 85 ventricular fibrillation in 20 children by transthoracic electric shock with continuous electrical current is studied. Initially an energy level of 2 W./sec./Kg., was used and obtained 95% of effectivity. 50% of patients were dead because they did not recover effective cardiac rhythm, in spite of the effectivity of desfibrillation. Authors evaluate the importance of correction of metabolic disturbances and hipoxemia as predisposing factors of ventricular fibrillation and success of treatment. They think that energy level of 2 W./sec./Kg., is efficient. Effectivity of therapy depends, mainly, on rapidity and training of the pediatric intensive care team.

Electric Countershock↗

PubMed1996

Modifications in the evolution of the dominant frequency in ventricular fibrillation induced by amiodarone, diltiazem, and flecainide. An experimental study.

In 22 anesthetized mongrel dogs, spectral methods were used to analyze the surface electrocardiogram (ECG) for the time course of the dominant frequency in ventricular fibrillation and its modifications under the influence of amiodarone, diltiazem, and flecainide. The ECG was recorded over 5 minutes after triggering ventricular fibrillation. Following A/D conversion and by applying the Fourier fast transform, the frequency spectrum of the signals was obtained. In group 1 (5 dogs), the ECGs were obtained without prior drug administration; group 2 (5 dogs) first received amiodarone, 5 mg/kg; group 3 (7 dogs) received diltiazem, 0.2 mg/kg; and group 4 (5 dogs) received flecainide, 2 mg/kg. All drugs were administered intravenously. An initial increase in the dominant frequency of ventricular fibrillation was found in the control group and also in the groups that received amiodarone, diltiazem, or flecainide. Diltiazem significantly increased the dominant frequency and diminished the arrhythmia-slowing process. Amiodarone and flecainide tended to diminish the dominant frequency.

Amiodarone↗

PubMed1982

[Prevention of ventricular fibrillation using lidocaine in the acute period of a myocardial infarct].

Two randomized investigations have shown a possibility to prevent primary ventricular fibrillation in acute myocardial infarction by lidocain. The first investigation was conducted in an intensive care unit on 316 patients hospitalized on an average 6 hours after the onset of acute myocardial infarction. 155 patients were included into a control group. Since the hospitalization 161 patients had been receiving lidocain (trimecain) intravenously and then intramuscularly for a day. The second investigation was conducted in accordance with the program "Myocardial Infarction Register" in a small town for 28 years. The sudden death rates among the patients who had been emergency cases within the first year were control. In subsequent 1.8 years all these patients received lidocain intramuscularly. The findings suggest that lidocain significantly reduces the incidence of primary ventricular fibrillation without suppressing ventricular rhythm disturbances completely.

Cardiac Complexes, Premature↗

PubMed1988

[Efficacy of verapamil in the prevention of ventricular fibrillation in the acute phase of myocardial infarction].

The effectiveness of verapamil in preventing ventricular fibrillation caused by coronary occlusion or reperfusion has been well demonstrated in animal studies, but these experimental data have not yet been confirmed in man. In this study we evaluated the prevalence of ventricular arrhythmias (fibrillation, sustained tachycardia and frequent extrasystoles) in patients hospitalized for myocardial infarction and treated with or without verapamil. The records of patients admitted to our Coronary Intensive Care unit during a 5-year period were analyzed retrospectively. Strict selection criteria enabled us to divide our patients into two homogeneous groups. The control group (group A) consisted of 106 patients who received only continuous infusions of heparin. The treated group (group B) comprised 89 patients who received exclusively verapamil by intravenous injections followed by continuous infusions. The prevalence of ventricular arrhythmia of all types was significantly lower in group B (22 p. 100) than in group A patients (71 p. 100; p less than 0.001). Episodes of ventricular fibrillation, in particular, were considerably less frequent in group B patients (1 p. 100) than in group A patients (13 p. 100; p less than 0.001). It would appear from these results that verapamil is highly effective in preventing death due to cardiac arrhythmia in the acute phase of myocardial infarction.

Cardiac Complexes, Premature↗

PubMed2000

Ventricular fibrillation threshold and local dispersion of refractoriness in isolated rabbit hearts with left ventricular dysfunction.

Patients with congestive heart failure or left ventricular dysfunction (LVD) have a high incidence of ventricular tachyarrhythmias and sudden cardiac death. In addition to structural, metabolic and neuroendocrine changes, mechanoelectrical feedback may play a role in arrhythmogenesis in heart failure. Three groups of rabbits (n = 10 for each) were studied: chronic coronary ligation with ejection fraction (EF) > or = 0.45 or < 0.45, and sham-operated controls. Ventricular fibrillation (VF) thresholds were measured at LV pressures of 0 and 40 mm Hg during modified Langendorff perfusion. Intervals between local activations during VF (VFI) were used as an index of refractoriness. Global dispersion was expressed as coefficient of variation of VFI; local dispersion by maximum difference in VFI between adjacent sites. Median VF threshold was lower at 0 mm Hg in the lower EF group compared to controls (30 vs. 67.5 mA, P<0.05). VF threshold in control hearts was lower at 40 mm Hg than at 0 mm Hg (P<0.01), but there was no further reduction in threshold in LVD hearts at 40 mm Hg. Global dispersion of VFI did not differ significantly between groups. Local dispersion of VFI in the lower EF group was greater than in controls at 0 mm Hg in the infarct border zone (P<0.05). At 40 mm Hg, local dispersion of VFI in zones bordering and remote from the infarct were greater in both LVD groups than in controls (P<0.05). Local inhomogeneity of refractoriness is more marked in the infarct border zone, but latent abnormalities are evident in normal myocardium of rabbits with left ventricular dysfunction and are revealed by left ventricular distension.

Animals↗

PubMed1984

Treatment of ventricular fibrillation. Emergency medical technician defibrillation and paramedic services.

We compared the effect of rapid defibrillation by emergency medical technicians (EMTs) combined with paramedic care with that of standard EMT and paramedic care on survival from 540 witnessed episodes of out-of-hospital cardiac arrest caused by ventricular fibrillation. More than 400 EMTs were trained in the recognition of ventricular fibrillation and operation of a defibrillator. For a portion of the three-year study, emergency care for 179 cases was randomized between the two types of services. For randomized cases, when the time interval between EMT and paramedic arrival was greater than four minutes there was significantly improved survival with EMT defibrillation and paramedic care (42%) compared with basic EMT and paramedic care (19%). Similar findings occurred when all cases were considered (38% v 18%). Defibrillation by EMTs combined with paramedic services can enhance survival from ventricular fibrillation, compared with basic EMT and paramedic care.

Aged↗

PubMed1979

Hospital resuscitation from ventricular fibrillation in Brighton.

The overall results over three and a half years of the treatment of ventricular fibrillation secondary to ischaemic heart disease in the Royal Sussex County Hospital were reviewed. Records of all patients who were brought to hospital by resuscitation ambulances or who were admitted to the coronary care unit from any source were analysed. Eighty-seven of the 174 patients (50%) who developed ventricular fibrillation were discharged. The survivors included 13 out of 61 patients (21%) in whom fibrillation was secondary to cardiogenic shock or severe left ventricular failure. The presence of resuscitation equipment and nursing staff trained to use it in the general wards and emergency areas ensured a uniformly high success rate throughout the hospital, similar to that achieved in the coronary care unit. Prompt defibrillation in the general wards and the accident and emergency department may improve overall survival.

Adult↗

PubMed1993

[Low energy cardioversion with the implantable cardioversion defibrillator devices for treatment of ventricular tachycardia and ventricular fibrillation].

Programmable implantable cardioverter-defibrillators (ICD) with low energy capabilities for the treatment of ventricular tachycardia were introduced to increase patients acceptance and lengthen battery life. However, no data about efficacy and safety of low energy cardioversion with subsequent defibrillation in ventricular tachycardia and fibrillation are available. Nineteen of 42 patients with documented or inducible ventricular tachycardia before ICD implantation were studied. In all patients the effectiveness of low-energy cardioversion (< or = 4 joules) with subsequent high-energy defibrillation was evaluated in monomorphic ventricular tachycardia and/or ventricular fibrillation. During predischarge programmed stimulation in 13/19 patients, a total of 32 monomorphic ventricular tachycardias occurred, and in only six patients could ventricular fibrillation be induced. A tachycardia-related efficacy of 69% and patient-related efficacy of 46% of the low-energy cardioversion < or = 4 joules was observed. Ten tachycardias were accelerated to ventricular fibrillation or remained unchanged (n = 2). The second shock (energy > 17 joules) terminated seven arrhythmias, whereas a third (30 joules) shock or an external defibrillation (n = 2) was necessary for termination of the remaining three arrhythmias. After induction of ventricular fibrillation as the primary arrhythmia, the first (low-energy) shock terminated 2/16 episodes, whereas the second (high-energy) shock reverted ventricular fibrillation in 11/16 episodes. In one patient, a second high energy shock and in two patients external defibrillation was necessary for conversion of ventricular fibrillation. In one patient, an increase of the defibrillation threshold induced by amiodarone could be identified.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2004

[Myocardial ischemic postconditioning: a brief ischemia causes conversion of resistent reperfusion-induced ventricular fibrillation into the normal rhythm].

Brief episodes of myocardial ischemia-reperfusion were shown to be protective against reperfusion injury when used during early reperfusion after a prolonged ischemic episode. This phenomenon has been termed myocardial ischemic postconditioning. In this study, an effect of ischemic postconditioning on persistent reperfusion-induced ventricular fibrillation was studied in the rat isolated heart. 2 minutes of global ischemia on the 15th minute of reperfusion after 30 minutes of regional ischemia effectively abolished the persistent ventricular fibrillation. In non-postconditioned hearts, the ventricular fibrillation continued to the end of reperfusion. The ischemic postconditioning seems to exert a strong antiarrhythmic effect protecting the heart against persistent reperfusion-induced ventricular tachyarrhythmias.

Animals↗

PubMed2006

Spontaneous polymorphic ventricular tachycardia after administration of pilsicainide in a patient resuscitated from ventricular fibrillation.

We performed a pilsicainide challenge test in a 38-year-old man who was resuscitated from ventricular fibrillation without apparent baseline electrocardiogram (ECG) abnormality. His father had a history of ventricular fibrillation and his brother had multiple episodes of syncope. Pilsicainide (1 mg/kg) induced short coupled ventricular premature beats followed by repetitive polymorphic ventricular tachycardia without apparent J wave and ST elevation, and excessive changes in QRS duration and QT interval. An implantable cardioverter defibrillator was implanted.

Adult↗

PubMedDate not supplied

Post-ischemic release of nucleosides and oxypurines in isolated rat hearts. Possible involvement of ventricular fibrillation.

In isolated perfused rat hearts global ischemia for 2, 5, and 15 min was produced. Depending on the duration of the ischemia, postischemic reperfusion led to the release of adenosine and its catabolites, and to more or less severe ventricular tachyarrhythmias. When ventricular fibrillation occurred, a highly significant increase in the purine release was observed compared with non-fibrillating hearts. Prevention of fibrillation by antiarrhythmic drugs decreased the purine release in a highly significant way. After only 2 min of ischemia, reperfusion did not lead to ventricular fibrillation. Electrical induction of fibrillation during the reperfusion in these hearts provoked the release of very high amounts of the purine compounds. A similar effect of electrically-induced fibrillation was also obtained in hearts without a previous ischemic period. The findings suggest that ventricular fibrillation is able to induce the release of purine derivatives from the heart.

Adenosine↗

PubMed1990

[Effectiveness of the methods of electric cardiac stimulation and low-energy cardioversion-defibrillation in the prevention and treatment of ventricular tachycardia and ventricular fibrillation].

The efficiency of treatment of ventricular tachycardias and fibrillation in cardiologic and cardiac surgical practice was examined in 154 patients by employing new unique means and facilities for automatic cardioversion-defibrillation of the heart. A comparative analysis was made of the efficiency of prevention of ventricular fibrillation and arrest of ventricular tachycardias by using various electric cardiac stimulation. The investigations indicated ventricular arrhythmia deaths might be significantly reduced by applying various methods of electric pulse therapy. The differential use of ++anti-tachycardia cardiac pacing and automatic low-energy cardioversion-defibrillation decreases the number of complications and enhances the efficiency of therapy in this contingent of patients.

Animals↗

PubMed1997

Adrenergic-dependent Effect of Adenosine-induced Ventricular Fibrillation in the Isolated Rabbit Heart.

BACKGROUND: The present study examined the contributory role of endogenous catecholamines in adenosine-induced ventricular fibrillation in isolation rabbit hearts. METHODS AND RESULTS: Cardiac catecholamine depletion was induced in eleven rabbits by the administration of 6-hydroxydopamine (2 x 30 mg/kg, every 12 hours intramuscularly). Hearts were removed 24 hours later, and subjected to 12 minutes of hypoxic perfusion followed by 40 minutes of reoxygenation while heart rate was maintained with atrial pacing. One of six, and one of five hearts from 6-hydroxydopamine treated rabbits developed ventricular fibrillation during hypoxia-reoxygenation when exposed to 3,7-dimethyl-1-propargylzanthine (DMPX) (10 µM) + adenosine (ADO) (1 µM) and DMPX (10 µM) + ADO (10 µM), respectively. In hearts from a control group, not exposed to 6-hydroxydopamine, ventricular fibrillation developed in each of five (100% incidence) hearts when perfused in the presence of DMPX (10 µM) + ADO (10 µM) (P <.05). Nadolol (1 µM), a beta-adrenoceptor DMPX (10 µM) + ADO (10 µM) treated hearts (n = 6, P <.05 vs DMPX + ADO treated hearts). To ensure catecholamine depletion, spontaneously beating isolated hearts from vehicle and 6-hydroxydopamine treated rabbits were perfused under normoxic conditions while exposed to increasing concentrations of tyramine (1, 3, 10 mM) and the change in heart rate was determined. A concentration-related, positive chronotorpic response to tyramine was obtained in hearts from the vehicle treated group that was absent in hearts from 6-hydroxy-dopamine treated rabbits or hearts perfused in the presence of nadolol. CONCLUSIONS: The results demonstrate that inhibition of the cardiac adenosine A(2) receptor, unmasks an adenosine A(1) receptor profibrillatory effect that is dependent upon endogenous cardiac catecholamines and beta-adrenoreceptor activation during myocardial hypoxia-reoxygenation.

Journal Article↗

PubMed2006

Effects of cocaine intoxication on the threshold for stun gun induction of ventricular fibrillation.

OBJECTIVES: This study sought to assess cocaine's effects on Taser-induced ventricular fibrillation (VF) threshold in a pig model. BACKGROUND: Stun guns are increasingly used by law enforcement officials to restrain violent subjects, who are frequently intoxicated with cocaine and other drugs of abuse. The interaction of cocaine and the stun gun on VF induction is unknown. METHODS: We tested five adult pigs using a custom device built to deliver multiples of standard neuromuscular incapacitating (NMI) discharge that matched the waveform of a commercially available electrical stun gun (Taser X-26, Taser International, Scottsdale, Arizona). The NMI discharges were applied in a step-up and step-down fashion at 5 body locations. End points included determination of maximum safe multiple, minimum VF-inducing multiple, and ventricular fibrillation threshold (VFT) before and after cocaine infusion. RESULTS: Standard NMI discharges (x1) did not cause VF at any of the 5 locations before or after cocaine infusion. The maximum safe multiple, minimum VF-inducing multiple, and VFT of NMI application increased with increasing electrode distance from the heart. There was a 1.5- to 2-fold increase in these values at each position after cocaine infusion, suggesting decreased cardiac vulnerability for VF. Cocaine increased the required strength of NMI discharge that caused 2:1 or 3:1 ventricular capture ratios at all of the positions. No significant changes in creatine kinase-MB and troponin-I were seen. CONCLUSIONS: Cocaine increased the VFT of NMI discharges at all dart locations tested and reduced cardiac vulnerability to VF. The application of cocaine increased the safety margin by 50% to 100% above the baseline safety margin.

Animals↗

PubMed1990

Effects of a thromboxane A2 synthetase inhibitor on ventricular fibrillation threshold during coronary artery occlusion and reperfusion.

The effects of a new thromboxane A2 synthetase inhibitor (DP-1904) on electrical stability of the heart were tested in anesthetized, open chest dogs. The incidence of spontaneous ventricular arrhythmias, ventricular refractory period and ventricular fibrillation threshold (VFT) during ligation of the left anterior descending coronary artery (LAD) for 180 min and after reperfusion were measured as indices of stability. Ventricular fibrillation and ventricular tachycardia occurred spontaneously after ligation of LAD in 56% of 9 control dogs and 29% of 7 dogs which received intravenous DP-1904 (100 mg) before ligation of LAD (n.s.). In the control group, the ventricular refractory period decreased in the ischemic region; consequently, the difference in refractory period duration between the ischemic and non-ischemic regions (i.e., dispersion) increased 30 min after coronary ligation (7 +/- 9 ms vs 32 +/- 17 ms, p less than 0.05). The dispersion at 30 min after coronary ligation, though, was not affected in the DP-1904 treated group (2 +/- 4 ms vs 10 +/- 9 ms, n.s.). The VFT (determined with pulse trains) decreased from 28 +/- 5 mA to 15 +/- 11 mA (p less than 0.05) 30 min after coronary ligation in the control group, but was not affected (30 +/- 0 mA vs 27 +/- 4 mA) in the DP-1904 group. The plasma concentration of thromboxane B2 decreased after DP-1904 administration (baseline vs 30 min after coronary ligation: 475 +/- 165 pg/ml vs 165 +/- 74 pg/ml, n = 3, p less than 0.05), while the concentration of 6-keto-prostaglandin F1 alpha increased gradually. In conclusion, DP-1904 prevents a decline in electrical stability in the ischemic region of the canine heart during coronary occlusion.

6-Ketoprostaglandin F1 alpha↗

PubMed2003

Ventricular fibrillation during anesthesia in association with J waves in the left precordial leads in a child with coarctation of the aorta.

A 14-year-old boy with coarctation of the aorta who showed repeat ventricular fibrillation during anesthesia, and ultimately sudden cardiac death in school, is presented. Electrocardiography showed J waves in the left precordial leads, which became prominent after an episode of ventricular fibrillation. While some of the clinical features and electrophysiological findings were similar to those seen in Brugada syndrome, others were inconsistent. J waves in the left precordial leads should be recognized as a possible waveform change inducing ventricular fibrillation predominantly at rest.

Adolescent↗