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PubMed1995

Adrenaline in out-of-hospital ventricular fibrillation. Does it make any difference?

BACKGROUND: A large proportion of cardiac arrests outside hospital are caused by ventricular fibrillation. Although it is frequently used, the exact role of treatment with adrenaline in these patients remains to be determined. AIM: To describe the proportion of patients with witnessed out-of-hospital cardiac arrest found in ventricular fibrillation who survived and were discharged from hospital in relation to whether they were treated with adrenaline prior to hospital admission. PATIENTS AND TREATMENT: All the patients with out-of-hospital cardiac arrest found in ventricular fibrillation in Göteborg between 1981 and 1992 in whom cardiopulmonary resuscitation (CPR) was initiated by our emergency medical service (EMS). During the observation period, some of the EMS staff were authorized to give medication and some were not. RESULTS: In all, 1360 patients were found in ventricular fibrillation and detailed information was available in 1203 cases (88%). Adrenaline was given in 417 cases (35%). Among patients with sustained ventricular fibrillation, those who received adrenaline experienced the return of spontaneous circulation more frequently (P < 0.001) and were hospitalized alive more frequently (P < 0.01). However, the rate of discharge from hospital did not differ significantly between the 2 groups. Among patients who converted to asystole or electromechanical dissociation, those who received adrenaline experienced the return of spontaneous circulation more frequently (P < 0.001) and were hospitalised alive more frequently (P < 0.001). However, the rate of discharge from hospital did not differ significantly between the 2 groups. CONCLUSIONS: On the basis of 2 treatment regimens during a 12-year survey, we explored the usefulness of adrenaline in out-of-hospital ventricular fibrillation. Both patients with sustained ventricular fibrillation and those who converted to asystole or electromechanical dissociation had an initially more favourable outcome if treated with adrenaline. However, the final outcome was not significantly affected. This study does not confirm the hypothesis that adrenaline increases survival among patients with out-of-hospital cardiac arrest who are found in ventricular fibrillation.

Aged↗

PubMed1992

Treatment of prolonged ventricular fibrillation. Immediate countershock versus high-dose epinephrine and CPR preceding countershock.

BACKGROUND: Early countershock of ventricular fibrillation has been shown to improve immediate and long-term outcome of cardiac arrest. However, a number of investigations in the laboratory and in the clinical population indicate that immediate countershock of prolonged ventricular fibrillation most commonly is followed by asystole or a nonperfusing spontaneous cardiac rhythm, neither of which rarely respond to current therapy. The use of epinephrine in doses greater than those currently recommended has recently been shown to improve both cerebral and myocardial perfusion during cardiopulmonary resuscitation (CPR). The purpose of this study was to compare cardiac resuscitation outcome between immediate countershock of prolonged ventricular fibrillation with high-dose epinephrine therapy and conventional CPR before countershock of prolonged ventricular fibrillation in a canine model. METHODS AND RESULTS: After sedation, intubation, induction of anesthesia, and instrumentation, ventricular fibrillation was electrically induced in 28 dogs. After 7.5 minutes of ventricular fibrillation, animals were randomly allocated to two treatment groups: group 1, immediate countershock followed by recommended advanced cardiac life support (ACLS) interventions, or group 2, 0.08 mg/kg epinephrine and manual closed-chest CPR before countershock and ACLS. In both groups, ACLS was continued until a spontaneous perfusing rhythm was restored or for 20 minutes (total arrest time, 27.5 minutes). A spontaneous perfusing rhythm was restored in three of 14 group 1 animals and in nine of 14 group 2 animals (p = 0.014 by sequential analysis method of Whitehead). Coronary perfusion pressure (aortic minus right atrial pressure during CPR diastole) before countershock was significantly greater in group 2 (21 +/- 7 mm Hg) when compared with mean circulatory pressure in group 1 (9 +/- 8, p less than 0.01). CONCLUSIONS: The findings of this study suggest that a brief period of myocardial perfusion before countershock improves cardiac resuscitation outcome from prolonged ventricular fibrillation.

Animals↗

PubMed1996

Effects of blockade of fast and slow inward current channels on ventricular fibrillation in the pig heart.

OBJECTIVE: To determine the contribution of fast and slow inward channels to the electrocardiogram (ECG) of ventricular fibrillation. METHODS: Ventricular fibrillation was induced by endocardial electrical stimulation in pigs anaesthetised with pentobarbitone sodium (30 mg/kg intravenously). ECGs simultaneously recorded from the body surface (lead II) and from the endocardium were studied by power spectrum analysis (0-40 Hz). RESULTS: The mean (SEM) dominant frequency of fibrillation (9.0 (1.1) Hz in lead II at 0-40 s) did not change significantly with time in pigs given intravenous saline. However, the dominant frequency was significantly reduced by intravenous pretreatment with the class I antiarrhythmic drugs, lignocaine (3 mg/kg, 6.5 (0.5) Hz; 10 mg/kg, 4.2 (0.6) Hz), mexiletine (3 mg/kg, 6.2 (0.4) Hz; 10 mg/kg, 5.5 (0.4) Hz), and disopyramide (2.5 mg/kg, 5.4 (0.6) Hz). After flecainide (3 mg/kg, 6.9 (0.5) Hz) the reduction in frequency was not significant. Similar data were obtained with endocardial recordings. In contrast pre-treatment with verapamil (0.2 mg/kg, 11.7 (0.8) Hz; and 1.0 mg/kg, 12.9 (1.6) Hz) produced a significantly higher dominant frequency of fibrillation than saline and widened the bandwidth of frequencies around the dominant frequency. CONCLUSIONS: These results indicate that voltage-dependent sodium channel currents contribute to the rapid frequencies of ventricular fibrillation. Blockade of L-type inward calcium channel activity increases the fibrillation frequency and fractionates the frequencies of the fibrillation wavefronts.

Animals↗

PubMed2003

Catheter Ablation of Ventricular Fibrillation in Structurally Normal Hearts Targeting the RVOT and Purkinje Ectopy.

Catheter ablation for ventricular fibrillation in structurally normal hearts is in its infancy. Recently, catheter ablation of idiopathic ventricular fibrillation as well as ventricular fibrillation associated with the long QT and Brugada syndromes has been described. This review article is a summary of our current understanding of the technique and results of catheter ablation of ventricular fibrillation in structurally normal hearts.

Adolescent↗

PubMed1989

Vitamin E and ventricular fibrillation threshold in myocardial ischemia.

The effect of vitamin E on the ventricular fibrillation threshold was studied in an experimental model of acute myocardial ischemia. An anterior thoracotomy was performed on 23 anesthetized Wistar rats. The ventricular fibrillation threshold was measured. Vitamin E was then administered intravenously to an experimental group (n = 11) and a placebo to a control group (n = 12). The ventricular fibrillation threshold was measured again. Finally, the left anterior descending coronary artery was occluded, producing anteroapical myocardial ischemia. The ventricular fibrillation threshold was measured again. This threshold did not vary significantly when vitamin E or the placebo was administered before occluding the coronary artery but after the occlusion a threshold decrease in the placebo group was observed, whereas no such decrease was manifested in the vitamin E-treated group. The results suggest that vitamin E prevents ventricular fibrillation in acute myocardial ischemia in rats.

Animals↗

PubMed1990

Fourier analysis of ventricular fibrillation of varied aetiology.

Fast Fourier Transform analysis was used to study ventricular fibrillation induced by several different methods in 43 greyhounds anaesthetized with sodium pentobarbitone. The dominant frequency at the body surface of ventricular fibrillation induced electrically in non-ischaemic hearts was initially 9.9 +/- 0.7 Hz, remained above 9 Hz for 70 s and then rapidly fell to 5 Hz. The dominant frequency of ventricular fibrillation induced by acute occlusion (initially 12.3 +/- 0.2 Hz), or by reperfusion (12.2 +/- 0.4 Hz) of the anterior descending branch of the left coronary artery, showed a similar time-course. However, ventricular fibrillation induced by administration of potassium (4.8 +/- 0.8 Hz) or ouabain (7.1 +/- 1.1 Hz) was significantly slower. Fibrillation recorded from the endocardium of the heart initially showed a similar dominant frequency to that recorded at the body surface, but there was no significant fall in frequency over 3.3 mins. There was little difference in the time-course of fibrillation in the non-ischaemic heart recorded directly from the epicardium or from a surface lead. These findings may be of relevance to the poor response to DC countershock after prolonged ventricular fibrillation, hyperkalaemia or cardiac glycosides.

Animals↗

PubMed1990

Calcium-dependent fluorescence transients during ventricular fibrillation.

Using surface fluorometry, calcium-dependent fluorescence transients were recorded during ventricular fibrillation in perfused rat and hamster hearts loaded with INDO 1-AM (fluorimetric reagent for calcium ion). Among a series of 203 consecutive isolated heart studies, 13 instances of ventricular fibrillation occurred. These arrhythmias developed during pretreatment with isoproterenol, dobutamine, norepinephrine, phenylephrine, digoxin, and 4 mmol/L calcium in the perfusate. Alternans behavior of calcium transients occurred in three cases; premature beats preceded ventricular fibrillation in six cases. Premature beats led to a further increase in the free intracellular calcium ([Ca2+]i) concentration, resulting in a stronger contraction with the subsequent beat and/or the initiation of ventricular fibrillation. Two distinct patterns of calcium transients were seen: ventricular fibrillation type 1 showed fast disorganized transients with small amplitude and an irregular, nonuniform tracing; type 2 revealed fast activity and multiform, polymorphous transients with marked changes in amplitude. Independent of the morphologic type of fibrillation, [Ca2+]i remained constant or even increased during an observation time up to 9 minutes. No intracellular hypocalcemia was observed. Isoproterenol pretreatment resulted in [Ca2+]i levels in the range of the end-diastolic calcium level of the last regular contraction. Fibrillating calcium transients after norepinephrine, dobutamine, phenylephrine, digoxin, high calcium, and fast pacing were in the previous end-systolic range. It is suggested that inotropic agents acting without a major elevation of cyclic adenosine monophosphate result in higher [Ca2+]i.

Animals↗

PubMed2003

Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized trial.

CONTEXT: Defibrillation as soon as possible is standard treatment for patients with ventricular fibrillation. A nonrandomized study indicates that after a few minutes of ventricular fibrillation, delaying defibrillation to give cardiopulmonary resuscitation (CPR) first might improve the outcome. OBJECTIVE: To determine the effects of CPR before defibrillation on outcome in patients with ventricular fibrillation and with response times either up to or longer than 5 minutes. DESIGN, SETTING, AND PATIENTS: Randomized trial of 200 patients with out-of-hospital ventricular fibrillation in Oslo, Norway, between June 1998 and May 2001. Patients received either standard care with immediate defibrillation (n = 96) or CPR first with 3 minutes of basic CPR by ambulance personnel prior to defibrillation (n = 104). If initial defibrillation was unsuccessful, the standard group received 1 minute of CPR before additional defibrillation attempts compared with 3 minutes in the CPR first group. MAIN OUTCOME MEASURE: Primary end point was survival to hospital discharge. Secondary end points were hospital admission with return of spontaneous circulation (ROSC), 1-year survival, and neurological outcome. A prespecified analysis examined subgroups with response times either up to or longer than 5 minutes. RESULTS: In the standard group, 14 (15%) of 96 patients survived to hospital discharge vs 23 (22%) of 104 in the CPR first group (P =.17). There were no differences in ROSC rates between the standard group (56% [58/104]) and the CPR first group (46% [44/96]; P =.16); or in 1-year survival (20% [21/104] and 15% [14/96], respectively; P =.30). In subgroup analysis for patients with ambulance response times of either up to 5 minutes or shorter, there were no differences in any outcome variables between the CPR first group (n = 40) and the standard group (n = 41). For patients with response intervals of longer than 5 minutes, more patients achieved ROSC in the CPR first group (58% [37/64]) compared with the standard group (38% [21/55]; odds ratio [OR], 2.22; 95% confidence interval [CI], 1.06-4.63; P =.04); survival to hospital discharge (22% [14/64] vs 4% [2/55]; OR, 7.42; 95% CI, 1.61-34.3; P =.006); and 1-year survival (20% [13/64] vs 4% [2/55]; OR, 6.76; 95% CI, 1.42-31.4; P =.01). Thirty-three (89%) of 37 patients who survived to hospital discharge had no or minor reductions in neurological status with no difference between the groups. CONCLUSIONS: Compared with standard care for ventricular fibrillation, CPR first prior to defibrillation offered no advantage in improving outcomes for this entire study population or for patients with ambulance response times shorter than 5 minutes. However, the patients with ventricular fibrillation and ambulance response intervals longer than 5 minutes had better outcomes with CPR first before defibrillation was attempted. These results require confirmation in additional randomized trials.

Adult↗

PubMedDate not supplied

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↗

PubMed1994

The mechanism of termination of reentrant activity in ventricular fibrillation.

The reentrant wave fronts in ventricular fibrillation (VF) have only a limited life span. The mechanisms by which these reentrant wave fronts terminate are unknown. We performed computerized mapping studies in six open-chest dogs before and after right ventricular subendocardial ablation with Lugol's solution. Recordings were made with 56 bipolar electrodes separated by 3 mm. Baseline pacing was performed on the right side of the tissue to create parallel activation wave fronts. A premature 50-V shock of either anodal or cathodal polarity was given to a bar electrode on the upper edge of the tissue. Counterclockwise reentrant wave fronts and VF were induced both before (60 episodes) and after (57 episodes) subendocardial ablation with either anodal or cathodal shocks. Among these reentrant wave fronts, 8 episodes before and 10 episodes after ablation had over 10 rotations (P = NS). The reentrant wave fronts in other episodes terminated with an average of 3.2 +/- 1.9 rotations before and 3.1 +/- 1.8 rotations after the ablation (P = NS). The reentrant wave-front cycle length was 118 +/- 19 milliseconds before and 124 +/- 20 milliseconds after ablation (P = .001). Conduction block occurred when the wave front was traveling across the myocardial fibers. When conduction was blocked in these episodes, the leading edge of the reentrant wave front encountered tissue that had been excited within the past 58 +/- 12 milliseconds (range, 28 to 77 milliseconds), which corresponded to 47 +/- 12% of the preceding VF cycle length. This period was significantly shorter than the recovery period in the same region that had allowed conduction (91 +/- 19 milliseconds; range, 48 to 137 milliseconds), which corresponded to 72 +/- 18% of the preceding VF cycle length (P < .001). In nine episodes, reentrant wave-front activity terminated when wave fronts that had originated from outside the mapped tissue interfered with the reentrant pathways. Conclusions are as follows: (1) The refractory period of fibrillating ventricular muscle ranges from 48 to 77 milliseconds. Because the refractory period is much shorter than the VF cycle length, a large excitable gap is present in the reentrant circuit. The presence of a large excitable gap contributes to reentrant wave-front termination. (2) Myocardial fiber orientation is an important determinant of the site of conduction block. (3) Although subendocardial ablation slowed the wave-front propagation, it did not prevent the generation and the maintenance of reentry and VF.

Animals↗

PubMed1981

Serial electrophysiological studies in a young patient with recurrent ventricular fibrillation.

A 28-year-old male with recurrent episodes of ventricular fibrillation, which were initiated by very early ventricular premature depolarizations with a normal QT interval, was subjected to three consecutive electrophysiological studies. During the first study, which was carried out to test the efficacy of amiodarone treatment, no ventricular arrhythmias could be induced. While on amiodarone therapy, the patient experienced another syncopal episode and therefore a second electrophysiological study was done. In that study, ventricular fibrillation was induced by ventricular stimulation. During the third study, which was carried out in order to evaluate the effect of the addition of quinidine to the on-going amiodarone therapy, no more than three repetitive ventricular responses could be induced. The patient has been asymptomatic since the third study (fifteen months) with combined therapy of amiodarone and quinidine. The significance of the ability to induce ventricular fibrillation during an electrophysiological study is discussed as well as the value of such studies in determining the long-term efficacy of antiarrhythmic drug therapy.

Adult↗

PubMed1988

Calcium oscillations in digitalis-induced ventricular fibrillation: pathogenetic role and metabolic consequences in isolated ferret hearts.

The pathophysiology of the ventricular fibrillation that complicates digitalis intoxication was investigated. In this and other calcium-overload states, oscillations of the intracellular free calcium concentration ([Ca2+]i) have been implicated as the cause of ventricular tachyarrhythmias. We addressed two questions: 1) Are [Ca2+]i oscillations obligatory in the pathogenesis of ventricular fibrillation during digitalis toxicity? 2) What are the metabolic consequences of [Ca2+]i oscillations? Ferret hearts (n = 20) were Langendorff-perfused at constant flow with oxygenated HEPES-buffered Tyrode's solution at 37 degrees C. Isovolumic left ventricular pressure was measured along with the extracellular electrogram or with simultaneous phosphorus nuclear magnetic resonance spectra. When strophanthidin (20 microM) was added during pacing at 3 Hz, the positive inotropic effect soon gave way to a decrease in developed force. The decrease in force was accompanied by an increase in inorganic phosphate concentration, a decrease in phosphocreatine concentration, and a slight acidosis. The rhythm changed to ventricular fibrillation after 12-25 minutes. This change was initially accompanied by further metabolic deterioration, but all metabolites reached steady state within 12-18 minutes of the onset of ventricular fibrillation. Fast Fourier transformation revealed the existence of periodic oscillations at 7-10 Hz in both the extracellular electrogram and the ventricular pressure during ventricular fibrillation. Ryanodine, an inhibitor of [Ca2+]i oscillations, abolished the pressure oscillations but not the voltage oscillations. Exposure to ryanodine significantly decreased the inorganic phosphate concentration and increased the phosphocreatine concentration (p less than 0.05) despite continuing exposure to strophanthidin. The results indicate that oscillations of [Ca2+]i are not required to sustain ventricular fibrillation, but when present, such oscillations contribute importantly to metabolic deterioration.

Animals↗

PubMed1989

Ventricular fibrillation in six adults without overt heart disease.

Findings are described in six patients with no clinical evidence of heart disease who had documented ventricular fibrillation (five patients) or ventricular flutter (one patient). The mean age of the six patients, all men, was 34 years (range 26 to 43). Cardiovascular collapse occurred in all and was followed by successful cardioversion. No patient had electrolyte or QT abnormalities. One patient had slight right ventricular enlargement on M-mode echocardiography, and another had a left ventricular pressure gradient at rest of 30 mm Hg with a normal two-dimensional echocardiogram. Holter electrocardiographic monitoring revealed incessant ventricular tachycardia in one patient and nonsustained ventricular tachycardia in three others. Exercise testing revealed nonsustained ventricular tachycardia in one patient. Ventricular fibrillation was induced at the time of programmed electrical stimulation in four of the six patients. Documented recurrence of ventricular fibrillation or ventricular flutter occurred in three patients, but in only one patient receiving antiarrhythmic drugs. Four patients were treated with amiodarone and one received an automatic implantable cardioverter-defibrillator. All patients are alive after a mean follow-up period of 78 months after the first documentation of their arrhythmia and 37 months after programmed electrical stimulation. Ventricular fibrillation can occur in the apparently structurally normal human heart. Antiarrhythmic treatment can provide effective control of this malignant arrhythmia.

Adult↗

PubMedDate not supplied

[Progressive decrease of the causes that maintain ventricular fibrillation after experimental coronary occlusion].

Progressive diminution of the causes that maintain ventricular fibrillation after coronary occlusion. Extracorporeal circulation was performed on a group of normal dogs in which a ligature was placed on the left anterior descending coronary artery, immediately beneath the bifurcation of the left coronary artery. The incidence of ventricular fibrillation was of 15 dogs out of 20 (table 1). In a control group without extracorporeal circulation ventricular fibrillation appeared in 24 dogs out of 30 (table 2). These results demonstrate that extracorporeal circulation performed with the idea of improving coronary circulation does not prevent ventricular fibrillation in coronary occlusion. In those dogs with the cross circulation, attempts to defibrillate the ventricles with an electric a.c. defibrillator (three electrical shocks applied directly on the myocardium every 4 or 5 minutes) were uniformly unsuccessful until a period ranging from 12 to 80 minutes elapsed after the onset of ventricular fibrillation. After these periods all fibrillating dogs were defibrillated and recovered either normal or idioventricular rhythm. It is assumed that a "fibrillator substance" liberated by the injury in the initial state of infarction is washed out of the myocardium, or a zone of increased excitability and conduction disturbance is progressively eliminated so that the chances of originating circus movements are diminished.

Animals↗

PubMed1995

Myocardial metabolic changes during reperfusion of ventricular fibrillation: a 31P nuclear magnetic resonance study in swine.

OBJECTIVE: Myocardial metabolic requirements during reperfusion of ventricular fibrillation are poorly understood. The objective of this study was to determine if controlled reperfusion after a clinically relevant global ischemia period of 10 mins was sufficient to prevent or reverse myocardial ischemia as indicated by changes in myocardial high energy phosphates, myocardial intracellular pH, and great cardiac vein lactate. DESIGN: Prospective laboratory study with controlled reperfusion. SETTING: Research laboratory at a university medical center. SUBJECTS: Five swine weighing 19 +/- 3 kg. INTERVENTIONS: Ten minutes of nonperfused ventricular fibrillation followed by reperfusion with cardiopulmonary bypass (flow 30 mL/kg/min) for 50 mins. MEASUREMENTS AND MAIN RESULTS: Myocardial adenosine triphosphate (ATP), phosphocreatine, and intracellular pH were determined using in vivo 31P nuclear magnetic resonance. Myocardial blood flow, measured by 15-mu radiolabeled microspheres, was significantly increased above baseline during reperfusion. Phosphocreatine was depleted during the 10 mins of nonperfused ventricular fibrillation, but recovered to 122 +/- 18% of baseline with reperfusion and was 112 +/- 18% at 60 mins (p < .005). ATP concentrations decreased to 51 +/- 16% of baseline after 10 mins of nonperfused ventricular fibrillation, improved to 67 +/- 9% of baseline with early reperfusion, and were 65 +/- 9% of baseline at 60 mins (p < .02). Myocardial intracellular pH improved from 6.11 +/- 0.18 after 10 mins of nonperfused ventricular fibrillation, to 6.89 +/- 0.20 with early reperfusion, and then decreased to 6.85 +/- 0.35 at 60 mins ventricular fibrillation (p < .001). Despite myocardial blood flows higher than baseline during the reperfusion period, great cardiac vein/aortic lactate gradient increased over the reperfusion period. CONCLUSION: Prolonged reperfusion with supranormal myocardial blood flow does not restore normal myocardial aerobic metabolism in the fibrillating myocardium after a 10-min nonperfused ventricular fibrillation period.

Adenosine Triphosphate↗

PubMed1983

Relationship between sympathetic neural activity, coronary dynamics, and vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion.

The relationship between neural sympathetic discharge and vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion was studied in 26 chloralose-anesthetized dogs. Preganglionic cardiac sympathetic impulse activity and ventricular fibrillation thresholds were separately determined before and during a 10-minute period of left anterior descending coronary artery occlusion and during release-reperfusion. Within 2 minutes of occlusion the ventricular fibrillation threshold was significantly decreased (from 25 +/- 1.3 to 16 +/- 2.3 mA, p less than 0.05) corresponding with the period of maximal activation of cardiac sympathetic preganglionic fibers (from 4.4 +/- 0.2 to 6.3 +/- 0.5 impulses/sec). Coronary sinus blood flow and oxygen tension decreased significantly. All these changes persisted for 5 to 6 minutes, thereafter returning to control levels despite continued obstruction of the coronary artery. A transient but significant reduction in ventricular fibrillation threshold also occurred with release of the occlusion but was unaccompanied by increases in sympathetic neural discharge. Bilateral stellectomy completely prevented the ventricular fibrillation threshold changes observed during coronary artery occlusion. However, there was no change in coronary sinus oxygen tension or blood flow. During reperfusion, stellectomy increased rather than decreased vulnerability to ventricular fibrillation. Stellectomy augmented the reactive hyperemic response to release-reperfusion. These findings indicate that enhanced cardiac sympathetic neural activity contributes to ventricular vulnerability associated with coronary artery obstruction. An opposite action results during release-reperfusion. Cardiac sympathetic neural discharge, by reducing the magnitude of reactive hyperemic response through influence on coronary vascular tone, exerts an antifibrillatory effect.

Animals↗

PubMed1996

[Value of calcium channel blockers in the prevention of ventricular fibrillation of ischemic etiology: experimental arguments].

The prevention of ventricular fibrillation raises a special problem when related to myocardial ischaemia, since class I antiarrhythmic drugs are then ineffective and may even behave as profibrillatory agents: the usual antifibrillatory properties of these drugs which are inhibitors of sodium channel, activated at high potentials, disappear with the disappearance of the role of sodium channel caused by ischaemic depolarization. Calcium channel then replacing sodium channel, calcium channel inhibitors should tend to prevent ischaemic ventricular fibrillation. Therefore, vulnerability to ventricular fibrillation was assessed in open-chest pigs by the threshold for fibrillation electrically induced with impulses of 100 ms duration at the rate of 180 beats/min. Ischaemia was produced by total occlusion of the left anterior descending coronary artery near its origin. Electrical fibrillation threshold was measured at the end of ischaemic period of increasing duration (30, 60, 120, 180, 240, 360 s) under control conditions and after i.v. administration of verapamil (50 micrograms/kg loading dose and 2 micrograms/kg/min infusion). Unaffected by verapamil when coronary circulation was normal, fibrillation threshold was raised by the drug when lowered by ischaemia, increasingly with the prolongation of ischaemia responsible for depolarization of the fibres, up to 500%. The rise of fibrillation threshold resulted in a delay in the triggering of fibrillation which occurs when the fibrillation threshold (6-8 mA) falls down to the pacing threshold (0.3-0.4 mA). These experiments tend to confirm the positive results recently obtained in man with verapamil in the prevention of postinfarction sudden death, provided that myocardial contractility is not too much adversely affected. But, in these experiments, left ventricular dP/dt max was not reduced by more than 15%, even just after the loading dose and returned to its control values within a few minutes.

Animals↗

PubMed1996

Localized right ventricular structural abnormalities in patients with idiopathic ventricular fibrillation: magnetic resonance imaging study.

Lethal arrhythmias, including ventricular tachycardia and ventricular fibrillation, may occur in the absence of apparent morphological abnormalities. However, a recent study using magnetic resonance imaging (MRI) has suggested that localized, minor structural abnormalities of the right ventricle are responsible for right ventricular outflow tract ventricular tachycardia in a number of patients. We demonstrated regional wall thinning and systolic dyskinesia of the right ventricle by MRI in two patients with idiopathic ventricular fibrillation in whom other cardiac imaging modalities failed to show abnormalities. This finding implies that minor structural abnormalities do exist in patients with so-called idiopathic ventricular fibrillation.

Adult↗