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PubMed2000

A mechanism of transition from ventricular fibrillation to tachycardia : effect of calcium channel blockade on the dynamics of rotating waves.

Abbreviation of the action potential duration and/or effective refractory period (ERP) is thought to decrease the cycle length of reentrant arrhythmias. Verapamil, however, paradoxically converts ventricular fibrillation (VF) to ventricular tachycardia (VT), despite reducing the ERP. This mechanism remains unclear. We hypothesize that the size and the dynamics of the core of rotating waves, in addition to the ERP, influence the arrhythmia manifestation (ie, VF or VT). The objectives of this study were (1) to demonstrate functional reentry as a mechanism of VF and VT in the isolated Langendorff-perfused rabbit heart in the absence of an electromechanical uncoupler and (2) to elucidate the mechanism of verapamil-induced conversion of VF to VT. We used high-resolution video imaging with a fluorescent dye, ECG, frequency and 2-dimensional phase analysis, and computer simulations. Activation patterns in 10 hearts were studied during control, verapamil perfusion (2x10(-6) mol/L), and washout. The dominant frequency of VF decreased from 16.2+/-0.7 to 13.5+/-0.6 Hz at 20 minutes of verapamil perfusion (P<0.007). Concomitantly, phase analysis revealed that wavefront fragmentation was reduced, as demonstrated by a 3-fold reduction in the density of phase singularities (PSs) on the ventricular epicardial surface (PS density: control, 1.04+/-0.12 PSs/cm(2); verapamil, 0.32+/-0.06 PSs/cm(2) [P=0.0008]). On washout, the dominant frequency and the PS density increased, and the arrhythmia reverted to VF. The core area of transiently appearing rotors significantly increased during verapamil perfusion (control, 4.5+/-0.6 mm(2); verapamil, 9.2+/-0.5 mm(2) [P=0.0002]). In computer simulations, blockade of slow inward current also caused an increase in the core size. Rotating waves underlie VF and VT in the isolated rabbit heart. Verapamil-induced VF-to-VT conversion is most likely due to a reduction in the frequency of rotors and a decrease in wavefront fragmentation that lessens fibrillatory propagation away from the rotor.

Animals↗
PubMed1997

Treatment of ventricular fibrillation during anaesthesia in an anaesthesia simulator.

BACKGROUND: To evaluate treatment of ventricular fibrillation (VF) occurring during anaesthesia and the use of a full-scale simulator, 80 anaesthetists in teams of two were attending a training session in the simulator Sophus. METHODS: The sessions were recorded on videotape and reviewed with the anaesthetists afterwards. Time of treatment and the sequence were registered. RESULTS: Onset time for VF was the starting point. Most of the subjects changed respiratory settings. Four teams did not change inspiratory oxygen and 17 teams did not turn off the vaporiser. Cardiac compression was initiated by all teams. DC-defibrillation was not used by two teams, with 38 of 40 teams defibrillating once, 37 twice and 29 teams three times. Adrenaline was administered by 30 of 40 teams. CONCLUSION: There was very little consistency among the teams regarding treatment for VF according to accepted algorithms. An anaesthesia simulator could be a tool for training and it is a safe way of demonstrating for the anaesthetist that certain treatment algorithms and behaviour during critical incidents are the most effective.

Anesthesia↗
PubMed1991

Frequency analysis of the human and swine electrocardiogram during ventricular fibrillation.

Recent studies in swine have suggested that estimating the duration of ventricular fibrillation (VF) could have important implications regarding the selection of the best therapeutic intervention during cardiopulmonary resuscitation (CPR). Successful defibrillation resulting in a pulsatile rhythm is more likely with VF of short duration, whereas VF of longer duration may require interventions designed to augment myocardial blood flow prior to defibrillation. Duration of VF has been estimated in a swine model by modelling the median frequency (FM) of the VF ECG signal. The purpose of this study was to characterize the time course of the FM ECG signal in humans during VF and compare the characteristics of the human VF ECG signal to that previously described in swine. Seven two-channel human VF ECG recordings were analyzed via fast Fourier transformation. The FM was extracted from each four-second segment of the recordings and plotted versus time. The FM in humans followed a repeatable time course during VF. The human data revealed an FM which had two peaks with subsequent gradual decline. The data in swine revealed an FM during VF which decreased initially then increased to a peak followed by a gradual decline. Our preliminary results demonstrate that a characteristic median frequency exists in humans which could be used to estimate the duration of VF.

Animals↗
PubMed1993

Frequency and prognostic significance of secondary ventricular fibrillation complicating acute myocardial infarction. SPRINT Study Group.

The incidence of secondary ventricular fibrillation (VF) complicating acute myocardial infarction (AMI) was 2.4% in a large cohort of unselected patients with AMI (142 of 5,839). Secondary VF was more frequent in patients with recurrent AMI (4%) than in those with a first AMI (1.9%) (p < 0.01). The hospital course was more complicated and in-hospital mortality was significantly higher in patients with secondary VF than in those with the same clinical hemodynamic condition but without VF (56 vs 16%; p < 0.0001). Multivariate analyses confirmed secondary VF complicating AMI as an independent predictor of high in-hospital mortality, with an odds ratio of 7 (95% confidence interval 4.6-10.6). However, long-term mortality after discharge (mean follow-up 5.5 years) was not increased in patients with as compared with those without secondary VF (39 vs 42%). These findings were also true when patients receiving beta blockers and antiarrhythmic therapy were excluded from analysis. Thus, this life-threatening arrhythmia occurring during hospitalization is not a marker of recurrent susceptibility to VF or an indicator of increased mortality after discharge from the hospital.

Aged↗
PubMed2004

Shock-induced epicardial and endocardial virtual electrodes leading to ventricular fibrillation via reentry, graded responses, and transmural activation.

INTRODUCTION: The mechanism of ventricular fibrillation (VF) induction by T wave shocks has been attributed to reentry, propagated graded responses (PGR), and triggered activity. The limitation of recording transmembrane potential (V(m)) from only a single surface has hampered efforts to elucidate the relative role of these phenomena and their relationship to shock-induced virtual electrodes. METHODS AND RESULTS: V(m) patterns from epicardial and endocardial surfaces of isolated sheep right ventricles were recorded with two CCD cameras for monophasic (M) and biphasic (B) shocks delivered at various coupling intervals (CI) from a unipolar mesh electrode on the epicardium. VF was induced via (1) the formation of reentry following make or break excitation; (2) propagated graded responses during apparent isoelectric window; and (3) breakthrough activation patterns coincident with endocardial-to-epicardial gradients in V(m). M shocks depolarized both surfaces at long CIs and polarized epicardial and endocardial surfaces oppositely at short CIs. At intermediate CIs, postshock V(m) patterns could lead to reentry on one surface or endocardial-to-epicardial gradients resulting in breakthrough. B induced VF less than M for short and intermediate CIs due to more homogeneous end-shock V(m) patterns. However, at long CIs these homogeneous patterns resulted in more VF induction because B left the tissue closer to the V(m) threshold for propagation. CONCLUSION: Postshock activity occurred either immediately via epicardial or endocardial reentry, or after a delay caused by transmural propagation or propagated graded responses. These findings could explain the isoelectric window and focal activation patterns observed on the epicardium following VF induction shocks.

Action Potentials↗
PubMed2002

[Ventricular fibrillation in a 27-year-old patient with heart contusion].

BACKGROUND: Patients with a blunt chest trauma often sustain myocardial contusion. The spectrum of symptoms varies from regional myocardial dysfunction to myocardial rupture or sudden cardiac death. CASE REPORT: After a kick against his chest, a 27-year-old patient was resuscitated because of ventricular fibrillation. ECG and enzymatic pattern corresponded to an acute myocardial infarction, the echocardiogram revealed an apical and anteroseptal hypokinesia. 10 days after the acute event, coronary arteriography and ventriculography did not show any abnormalities. CONCLUSION: On the basis of the anamnesis, a myocardial contusion must be discussed as reason for the ventricular fibrillation and the pathologic findings in ECG and echocardiogram. This has to be considered in the therapy.

Adult↗
PubMed1993

Effects of monophasic and biphasic shocks on action potentials during ventricular fibrillation in dogs.

This study determined the response of action potentials during ventricular fibrillation (VF) to timed monophasic and biphasic shocks. A floating glass microelectrode was used to record intracellularly from the anterior right ventricle in 10 open-chest dogs. After 10 seconds of electrically induced VF, 5-millisecond monophasic and 2.5/2.5-millisecond biphasic shocks or 16-millisecond monophasic and 8/8-millisecond biphasic shocks were given via mesh electrodes on either side of the microelectrode. Monophasic and biphasic truncated exponential shocks of 5 V/cm were given with coupling intervals timed from the beginning of a VF action potential to the shock ranging from 50 to 70 milliseconds in 5-millisecond increments. Each coupling interval for each waveform was tested during a different VF episode. The interval between successive activations during VF was 86 +/- 15 milliseconds (mean +/- SD). The refractory period during VF was 61 +/- 5 milliseconds for 5-millisecond monophasic shocks and 66 +/- 6 milliseconds for 2.5/2.5-millisecond biphasic shocks (P < .05). At each coupling interval, action potential duration at 50% repolarization (APD50) was significantly prolonged by the shocks compared with the mean preshock APD50 (P < .05). ADP50 duration increased significantly with increases in the coupling interval (P < .05) for both monophasic and biphasic waveforms. For all coupling intervals together, APD50 prolongation as a percent of the mean preshock APD50 was 170 +/- 55%, 192 +/- 45%, 151 +/- 44%, and 175 +/- 45% for 5- and 16-millisecond monophasic and 2.5/2.5- and 8/8-millisecond biphasic waveforms, respectively. This APD50 prolongation was greater for monophasic than biphasic shocks and was greater for longer than shorter waveforms (P < .05). Thus, during VF, (1) the refractory period for 5-V/cm truncated exponential waveforms lasting 5 milliseconds is approximately 75% of the VF activation interval; (2) the refractory period is shorter for monophasic than for comparable biphasic waveforms; (3) both monophasic and biphasic 5-V/cm shock fields cause prolongation of action potential duration; (4) prolongation of action potential duration increases as the coupling interval increases; and (5) prolongation of action potential duration is greater for monophasic shocks and for longer shock waveforms.

Action Potentials↗
PubMed2005

Better outcome after pediatric defibrillation dosage than adult dosage in a swine model of pediatric ventricular fibrillation.

OBJECTIVES: This study was designed to compare outcome after adult defibrillation dosing versus pediatric dosing in a piglet model of prolonged prehospital ventricular fibrillation (VF). BACKGROUND: Weight-based 2 to 4 J/kg monophasic defibrillation dosing is recommended for children in VF, but impractical for automated external defibrillator (AED) use. Present AEDs can only provide adult shock doses or newly developed attenuated adult doses intended for children. A single escalating energy sequence (50/75/86 J) of attenuated adult-dose biphasic shocks (pediatric dosing) is at least as effective as escalating monophasic weight-based dosing for prolonged VF in piglets, but this approach has not been compared to standard adult biphasic dosing. METHODS: Following 7 min of untreated VF, piglets weighing 13 to 26 kg (19 +/- 1 kg) received either biphasic 50/75/86 J (pediatric dose) or biphasic 200/300/360 J (adult dose) therapies during simulated prehospital life support. RESULTS: Return of spontaneous circulation was attained in 15 of 16 pediatric-dose piglets and 14 of 16 adult-dose piglets. Four hours postresuscitation, pediatric dosing resulted in fewer elevations of cardiac troponin T (0 of 12 piglets vs. 6 of 11 piglets, p = 0.005) and less depression of left ventricular ejection fraction (p < 0.05). Most importantly, more piglets survived to 24 h with good neurologic scores after pediatric shocks than adult shocks (13 of 16 piglets vs. 4 of 16 piglets, p = 0.004). CONCLUSIONS: In this model, pediatric shocks resulted in superior outcome compared with adult shocks. These data suggest that adult defibrillation dosing may be harmful to pediatric patients with VF and support the use of attenuating electrodes with adult biphasic AEDs to defibrillate children.

Age Factors↗
PubMed1995

Ventricular arrhythmias detected after transvenous defibrillator implantation in patients with a clinical history of only ventricular fibrillation. Implications for use of implantable defibrillator.

BACKGROUND: Patients with a history of ventricular fibrillation (VF) have been shown to have a clinical profile, response to electrophysiological testing (EPS), and response to antiarrhythmic therapy that distinguishes them from patients with a history of sustained monomorphic ventricular tachycardia (MVT). Despite these differences, it is not clear whether VF in these patients is triggered by MVT or occurs de novo. The incidence of MVT and VF in such patients after their index VF event has important implications for therapeutic decisions regarding implantable defibrillator selection and programming. METHODS AND RESULTS: The records of 111 consecutive patients who had undergone transvenous cardioverter/defibrillator (ICD) implantation for malignant ventricular arrhythmias were reviewed retrospectively. For each patient, all device tachyarrhythmia detections were examined and classified as VF, MVT, rapid polymorphic VT, or other. The number of events, time to first arrhythmia detection, and cycle length of MVTs were recorded. There were 55 patients with a history of only VF and 56 with a history that included an episode of MVT. Over 14 months of follow-up, with all patients initially off of antiarrhythmic medications, MVT was detected by only 18% of patients with a history of only VF compared with 54% of those with a history that included MVT (P = .002). Among patients who did detect MVT, those with a history of only VF had fewer episodes (7 +/- 7 versus 20 +/- 31, P = .001) and a shorter mean MVT cycle length (279 versus 314 ms, P = .03) than those with a clinical history of MVT. Abrupt onset of VF not preceded by MVT was detected in 11% of patients with VF only. In addition to a history of MVT, male sex, age < 60 years, and MVT inducible on EPS were all significantly associated with an increased likelihood of MVT detection. On multivariate analysis, the inducibility of MVT was the primary independent predictor of MVT detection but was of minimal incremental predictive value in the subgroup of patients with a history of only VF. When EPS results were not considered, arrhythmia history was the primary independent predictor of MVT detection. CONCLUSIONS: Patients with a history of only VF infrequently have MVT detected by their defibrillators. When these patients do detect MVT, it is faster than that detected in patients with a clinical history of MVT before ICD surgery. A significant percentage of VF survivors detected the abrupt onset of VF not preceded by MVT, suggesting that the deterioration of rapid MVT to VF is not the only clinically important mechanism of VF induction. These findings may have important implications for the understanding of the mechanism of VF induction and for use of an implantable defibrillator.

Cardiac Pacing, Artificial↗
PubMed2004

Genuine effects of ventricular fibrillation upon myocardial blood flow, metabolism and catecholamines in patients with aortic stenosis.

OBJECTIVE: Ventricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine concentrations in patients undergoing surgery for aortic stenosis. DESIGN: The immediate effects of up to 5 min of VF were studied in 21 patients during cardiopulmonary bypass (CPB) before valve replacement. RESULTS: During VF the global myocardial oxygen consumption, coronary blood flow and vascular resistance were unchanged, and the mean arterial pressure (on CPB) decreased from 70 to 51 mmHg (p < 0.02). Fibrillation induced a high myocardial tone and a probable functional aortic insufficiency, which instantly equilibrated left ventricular and aortic pressures. Signs of myocardial ischaemia and acidosis developed after 4 min: a decrease in the pH of coronary sinus blood from 7.38 to 7.32 (p < 0.001), an increased release of lactate from 32 to 137 micromol/min (p < 0.001) and potassium from 29 to 73 micromol/min (p < 0.05). The noradrenaline net release increased from 0.021 to 0.58 nmol/min (p < 0.02) after 1.5 min of VF and then decreased. The adrenaline net uptake remained low and unchanged (17-28%). CONCLUSION: VF in patients with aortic stenosis was rapidly followed by myocardial ischaemia, acidosis and a transient increase in the myocardial noradrenaline net release despite sufficient coronary perfusion and unchanged global myocardial oxygen consumption. The VF instantly induced equilibration of left ventricular and aortic pressure and probably caused a relative underperfusion of the subendocardium. These factors all support persistence of VF.

Adult↗
PubMedDate not supplied

Acute myocardial ischaemia in the anaesthetised pig: local catecholamine release and its relation to ventricular fibrillation.

In anaesthetised open-chest pigs, sequential myocardial samples were obtained before and after occlusion of the distal half of the LAD. These samples were analysed histofluorimetrically to determine the density of catecholamine containing neurones in each sample (quantified morphometrically), and radioenzymatically for total tissue noradrenaline content. Following coronary artery occlusion, 75% of the animals (24 out of 32) died in ventricular fibrillation in the first 30 min, the other 25% (8/32) survived the first 60 min of myocardial ischaemia. Coronary artery occlusion led to a significant reduction in the density of fluorescing fibres in the ischaemic myocardium of animals which fibrillated (from 1.25 +/- 0.2% to 0.67 +/- 0.10% at 15 min) whereas in the survivors there was no significant change in fluorescing area during the course of the experiment. Animals which fibrillated had a significant reduction in tissue noradrenaline concentration of the ischaemic myocardium (from an initial concentration of 612 +/- 72 to 402 +/- 64 ng/g ww) within the first 5 min of ischaemia. It is concluded that in this model of myocardial ischaemia, the development of ventricular fibrillation in the early phase seems to be related to the release of noradrenaline from the sympathetic neurones after the onset of myocardial ischaemia.

Animals↗
PubMed1994

Ventricular fibrillation in a patient with exercise-induced anaphylaxis, normal coronary arteries, and a positive ergonovine test.

Exercise-induced anaphylaxis (EIA) is a rare form of physical allergy. Although histamine release is a feature of EIA, and histamine provocation of coronary spasm has been described, serious cardiac arrhythmias in EIA have not been reported. Exercise-induced anaphylaxis was diagnosed in a survivor of out-of-hospital cardiac arrest due to ventricular fibrillation after ECG signs of coronary spasm. Coronary artery disease was excluded. Ergonovine provocation induced coronary spasm in this patient. This is, to the authors' knowledge, the first description of ventricular fibrillation in EIA, possibly due to coronary spasm.

Anaphylaxis↗
PubMed1994

[Initial defibrillation by emergency physicians or by first aid assistants? A prospective, comparative multicenter study in outpatients with ventricular fibrillation].

In a controlled prospective randomized study, defibrillation by emergency medical technicians (EMTs) was compared with the current standard of care in Germany (basic life support by EMTs and defibrillation by emergency physicians only) in order to answer the following questions: 1. Does EMT defibrillation improve the survival rate and long-term prognosis of patients in ventricular fibrillation as compared to the current German standards in resuscitation (basic life support by EMTs and defibrillation by emergency physicians)? 2. Are the prerequisites for the use of semiautomatic defibrillators fulfilled in the emergency medical systems (EMS) of the participating centers? METHODS. The study phase includes randomization of 121 adult patients with witnessed cardiac arrest and ventricular fibrillation (VF) as first ECG rhythm. Prior to the onset of the study, all EMTs of the participating EMS systems were retrained in basic life support (BLS) measures. In each center, randomly assessed EMT-Ds (EMTs trained in Defibrillation) were trained to use semiautomatic defibrillators. With the help of one-line tape recording, the time intervals during resuscitation and treatment steps were evaluated. Successfully resuscitated patients were followed up with the help of the Glasgow Coma Scale and the Pittsburgh Cerebral and Overall Performance Categories. RESULTS. From 1 February 1991 until 28 June 1992, 159 patients with VF were randomized. In 121 cases, collapse was witnessed. 25% (14/57) of the patients receiving defibrillation by EMT-Ds (study group = S) were discharged from the hospital alive. In the control group, 52 patients were defibrillated by emergency physicians, following BLS by EMTs [control group 1 = C1; discharged: 29% (15/52)]. Fifty patients received BLS and advanced cardiac life support (ACLS) by the emergency physicians crews [control group 2 = C2; discharged: 18% (9/20)]. In the study group, the median time interval from collapse of the patient until initiation of BLS measures was 7.7 min, 7 min in C1 and 8 min in C2. ACLS measures were initiated significantly earlier (P < 0.05) in the control groups, as compared to the study group [S: 13 min, C1: 11 min; C2: 10.3 min]. Sixty-seven percent (30/45) of the study patients and 46% (36/76) of the control patients were defibrillated within 12 min. Study patients were defibrillated earlier (P < 0.05) (S: 9.9 min; C1: 12.2 min; C2: 12.75 min); return of spontaneous circulation (ROSC) was achieved earlier (P < 0.05) in the study group [S: 14 min; C1: 19 min; C2: 18.2 min] and the number of patients in the study group requiring no epinephrine during resuscitation was higher (P < 0.01) than in the control groups [S: 35.3% (12/34); C1: 10% (4/40); C2: 10.5% (4/38)]. Furthermore, the total amount of epinephrine [mean (+/- standard error)] administered in the study group [S: 2.35 (+/- 0.49) mg; C1: 6.71 (+/- 0.98) mg; C2: 7.71 (+/- 1.31) mg] was significantly lower (P < 0.05). No significant differences in neurological long-term prognosis were found for the groups investigated. CONCLUSION. Neither the initial survival rate the number of patients discharged alive, nor the neurological long-term prognosis was significantly different for any of the groups investigated. Because of apparent differences in indirect prognostic parameters (time interval until ROSC, number of patients requiring no epinephrine) and because of the fact that the time interval to the first defibrillation was reduced by EMT defibrillation, EMT-Ds may perform defibrillation if: (a) they reach the patient before the emergency physician and (b) if they are trained intensively and supervised continuously. In order to increase the efficiency of defibrillation by EMT-Ds, far-reaching changes in our EMS are mandatory: (a) a reduction in the time interval from collapse until initiation of BCLS measures by intensifying layperson CPR training; (b) an increase in the number of emergency units equipped with semiautomatic defibril

Electric Countershock↗
PubMed1985

DOCA-salt induced myocardial sensitization to ventricular fibrillation by isoprenaline in rats. Role of the autonomic nervous system.

The possible role of the autonomic nervous system in the development of myocardial sensitization to isoprenaline produced by DOCA-salt pretreatment was evaluated in bilaterally unanaesthetized rats subject to chronic ganglionic blockade with chlorisondamine or hexamethonium and to treatment with 6-hydroxydopamine. Isoprenaline produced ventricular fibrillation and death in rats pretreated for 6 days with DOCA (20 mg pellet, s.c.) and 0.9% saline. The incidence of mortality was dose dependent and was 76.6% with 150 microgram/kg of isoprenaline. Adrenalectomy did not alter the mortality rate. The combination of adrenalectomy with concurrent chronic ganglionic blockade significantly decreased the incidence of mortality and delayed the time of death. In contrast, 6-hydroxydopamine treatment and adrenalectomy did not alter the incidence of mortality nor time of death. No differences in myocardial noradrenaline turnover were detected in rats susceptible and nonsusceptible to death in ventricular fibrillation. We conclude that myocardial sensitization to isoprenaline induced by DOCA-salt requires a neurogenic component, which is not, however, manifested by changes in myocardial noradrenaline turnover.

Adrenalectomy↗
PubMed2005

Phase singularities and filaments: simplifying complexity in computational models of ventricular fibrillation.

In the whole heart, millions of cardiac cells are involved in ventricular fibrillation (VF). Experimental studies indicate that VF is sustained by re-entrant activity, and that each re-entrant wave rotates around a filament of phase singularity. Filaments act as organising centres, and offer a way to simplify and quantify the complex spatio-temporal behaviour observed in VF. Where a filament touches the surface of fibrillating myocardium re-entrant activity can be observed, however the behaviour of filaments within bulk ventricular myocardium is difficult to observe directly using present experimental techniques. Large scale computational simulations of VF in three-dimensional (3D) tissue offer a tool to investigate the properties and behaviour of filaments, and the aim of this paper is to review recent advances in this area as well as to compare recent computational studies of fibrillation in whole ventricle geometries.

Animals↗
PubMed2003

Two-dimensional analysis of ventricular fibrillation in the guinea pig.

Cardiac arrhythmias are undesirable electrical activity in the heart. Ventricular fibrillation (VF) is a fatal cardiac arrhythmia and is characterized by the breakdown of organized electrical activity in the ventricular myocardium. However, little is known about VF, partially because it is difficult to study and understand an apparently disorganized activity. One method for discovering the nature of VF is processing the epicardial electrical signals by using cardiac mapping techniques. These techniques involve the study of propagation patterns seen in VF. In this project, we used guinea pigs to study the spatial organization of the epicardial electrical activity during VF. VF was induced in 9 open chest guinea pigs and epicardial electrode data were acquired by using a square array of 192 electrodes for 4 seconds every minute. The mean correlation length and dominant frequency were measured in each recorded segment. Correlation length is a measure of the spatial order in a system and dominant frequency is the frequency corresponding to the spectral maximum. The mean correlation length was found to vary between 1-7 mm and the dominant frequency was in the range of 1-14 Hz. This study suggests that guinea pig VF exhibits a level of organization equivalent to or greater than that seen in previous studies.

Analysis of Variance↗
PubMed1983

Intrinsic sympathomimetic activity and the effects of beta-adrenergic blocking drugs on vulnerability to ventricular fibrillation.

Beta-adrenergic blocking agents differ considerably in their effects on myocardial excitable properties. The possibility that intrinsic sympathomimetic activity might contribute to such differences has not been adequately explored. This study examined the influence of intrinsic sympathomimetic activity on the electrophysiologic effects of three agents with varying degrees of such activity. Intravenous propranolol (0.5 mg/kg), oxprenolol (0.5 mg/kg) and pindolol (0.05 mg/kg) were administered in 16 anesthetized dogs. The effects of the drugs on ventricular vulnerability were studied over a 2 hour period. Propranolol and oxprenolol raised the ventricular fibrillation threshold by 42 and 56%, respectively. In contrast, pindolol resulted in an elevation of only 25%. After depletion of endogenous norepinephrine stores using reserpine, pindolol led to a decrease of the ventricular fibrillation threshold, which was reversed by propranolol. These data indicate that intrinsic sympathomimetic activity of beta-adrenergic blocking agents substantially alters their ultimate effect on myocardial excitable properties.

Adrenergic beta-Antagonists↗