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PubMed2001

The beneficial effect of basic life support on ventricular fibrillation mean frequency and coronary perfusion pressure.

BACKGROUND AND OBJECTIVE: Chest compressions before initial defibrillation attempts have been shown to increase successful defibrillation. This animal study was designed to assess whether ventricular fibrillation mean frequency after 90 s of basic life support cardiopulmonary resuscitation (CPR) may be used as an indicator of coronary perfusion and mean arterial pressure during CPR. METHODS AND RESULTS: After 4 min of ventricular fibrillation cardiac arrest in a porcine model, CPR was performed manually for 3 min. Mean ventricular fibrillation frequency and amplitude, together with coronary perfusion and mean arterial pressure were measured before initiation of chest compressions, and after 90 s and 3 min of basic life support CPR. Increases in fibrillation mean frequency correlated with increases in coronary perfusion and mean arterial pressure after both 90 s (R=0.77, P<0.0001, n=30; R=0.75, P<0.0001, n=30, respectively) and 3 min (R=0.61, P<0.001, n=30; R=0.78, P<0.0001, n=30, respectively) of basic life support CPR. Increases in fibrillation mean amplitude correlated with increases in mean arterial pressure after both 90 s (R=0.46, P<0.01; n=30) and 3 min (R=0.42, P<0.05, n=30) of CPR. Correlation between fibrillation mean amplitude and coronary perfusion pressure was not significant both at 90 s and 3 min of CPR. CONCLUSIONS: In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.

Animals↗

PubMed1993

Management of hospital survivors of pre-hospital ventricular fibrillation.

The objective of our study was to characterise 52 hospital survivors of pre-hospital ventricular fibrillation and record their initial management in hospital. A retrospective review was undertaken of ambulance report forms, hospital notes, and electrocardiograms, in one teaching hospital and three district general hospitals in South Wales, of 53 patients discharged from hospital between February 1987 and April 1992 after resuscitation from pre-hospital ventricular fibrillation by ambulance personnel. Twenty patients showed evidence of acute myocardial infarction (group 1), eight patients had a diagnosis of 'possible acute myocardial infarction' (group 2), and 25 patients had no evidence of acute myocardial infarction (group 3). Nineteen patients in group 1 experienced chest pain before collapse compared with only six patients in group 3 (p < 0.001). Five patients in group 1 had a previous history of ischaemic heart disease compared with 17 patients in group 3 (p < 0.01). A greater proportion of patients in group 3 were taking diuretic medication (15 of 25 vs 4 of 20: p < 0.01) but there was no difference in potassium levels on admission to hospital. Cardiologists were involved in the management of a minority of patients (21 of 53); only eight patients underwent cardiac catheterisation; and only three were referred for electrophysiological studies. Patients in group 3 were more likely to be discharged taking empiric antiarrhythmic drugs (13 of 25) than patients in group 1 (2 of 20) (p < 0.01). Not enough use is made of noninvasive and invasive investigations in the management of survivors of pre-hospital ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2002

[Effects of myocardial stretching on excitation frequencies determined by spectral analysis during ventricular fibrillation].

INTRODUCTION AND OBJECTIVES: The aim of this study was to analyze the effects of myocardial stretching on excitation frequencies, as determined by spectral analysis, during ventricular fibrillation. METHODS: In 12 isolated rabbit heart preparations, ventricular activation during ventricular fibrillation was recorded with multiple electrodes. Recordings were obtained before, during and after ventricular dilatation produced with an intraventricular balloon. The dominant frequency of the signals obtained with each of the electrodes was determined by spectral analysis. RESULTS: During the control phase, the mean, minimum and maximum dominant frequencies were, respectively, 14.3 1.7, 12.5 1.7, and 16.2 1.4 Hz, and the average difference between the maximum and minimum frequencies was 3.6 2.1 Hz. This difference was over 4 Hz in four cases, and in no case did it exceed 8 Hz. During ventricular stretching, the mean dominant frequency increased significantly (21.1 6.1 Hz; p < 0.0001), as did the minimum values (14 2.6 Hz; p < 0.05) and especially the maximum values (26.6 7.7 Hz; p < 0.0001). The difference between the maximum and minimum frequencies (12.6 6.4 Hz; p < 0.001) was over 4 Hz in all cases except one, and over 8 Hz in 9 cases. The maximum values were distributed heterogeneously during ventricular stretching. Upon suppressing ventricular stretching, the dominant frequency did not differ from controls. CONCLUSIONS: Myocardial frequency maps during ventricular fibrillation show limited variations in the dominant frequency of the signals recorded in the lateral wall of the left ventricle. During stretching, the patterns were heterogeneous, due mainly to the marked increase in the maximum dominant frequency. In the experimental model used, the effects of stretching remitted after suppressing ventricular dilatation.

Animals↗

PubMed1995

Effects of chemical subendocardial ablation on activation rate gradient during ventricular fibrillation.

The mechanism by which an endocardial-epicardial activation rate gradient develops after 1 or 2 min of sustained ventricular fibrillation is unknown. We recorded from electrodes on the epicardium and from hook electrodes in the endocardium in three open-chest control dogs during prolonged ventricular fibrillation. The same recordings were also made in seven dogs after right ventricular subendocardial ablation with Lugol solution and in three dogs after substitution of air for the cavitary blood. The effects of these interventions, i.e., Lugol ablation (n = 2) and the exposure to air (n = 2), on the subendocardial Purkinje fiber transmembrane action potential properties were also evaluated in vitro using microelectrode recording techniques. The in vivo studies showed a significant endocardial-epicardial rate gradient in the control dogs and in dogs that had air substituted for the cavitary blood. In comparison, in dogs that underwent chemical subendocardial ablation, the activation cycle lengths for the endocardium and epicardium were not significantly different. The in vitro studies showed that subendocardial Purkinje fiber action potentials could still be recorded for up to 10 min of exposure to air. In comparison, in the tissues subjected to chemical ablation, no transmembrane action potentials could be recorded from either the Purkinje fibers or superficial ventricular muscle cells. We conclude that the development of an endocardial-epicardial activation rate gradient during prolonged ventricular fibrillation depends on the presence of intact subendocardial Purkinje fibers and ventricular myocytes. The retained cavitary blood is not responsible for the development of the rate gradient.

Animals↗

PubMed1994

Complex dynamic order in ventricular fibrillation.

Self-sustained circus movement of excitation has long been discussed as the underlying mechanism of ventricular fibrillation. This concept now appears to have found general acceptance. Mapping studies are very expensive and do not permit observations to be isolated from varying external influences. The authors have therefore used a simple cellular automation for studying the basic principles of excitation spreading during ventricular fibrillation under various conditions. Highly ordered spiral waves, described in other computer models, previously interpreted as fibrillation were encountered. Comparisons of pseudo-electrocardiograms created by the cellular automaton with original electrocardiographic recordings showed similarity in the time series and in fast Fouriér transformation. Modulation of refractory times often led to the termination of model fibrillation. Clinical evidence suggests that maintenance of the 1/f (RR-variability) variations produced by the autonomic nervous system exerts a protective effect on the evolution of ventricular fibrillation.

Computer Simulation↗

PubMed2005

May fever trigger ventricular fibrillation?

The clinical precipitants of ventricular fibrillation (VF) remain poorly understood. Clinical factors such as hypoxemia, acidosis or electrolyte imbalance, drug-related toxicity, autonomic nervous system disorders as well as viral myocarditis have been proposed to be associated with sudden cardiac death particularly in patients with structural heart disease. However, In the Brugada syndrome, concurrent febrile illness has been reported to unmask the electrocardiographic features of the Brugada syndrome and be associated with an increased propensity for VF. More recently, a febrile illnesses of infectious etiology was associated to polymorphic ventricular tachycardia or VF in patients with normal hearts and without known repolarization abnormality. In this review we detail this phenomenon and its putative mechanisms.

Journal Article↗

PubMed2007

Bi-ventricular circulatory support with the Abiomed AB5000 system in a patient with idiopathic refractory ventricular fibrillation.

A 45-year-old man had life-threatening recurrent idiopathic ventricular fibrillation and persistent cardiogenic shock develop. The episodes of ventricular fibrillation were refractory to aggressive medical management; therefore an Abiomed AB5000 bi-ventricular support system was implanted for arrhythmia control. The device was able to maintain hemodynamic stability during the following 2 weeks. The patient was discharged from the hospital with fully recovered cardiac function.

Heart-Assist Devices↗

PubMed1987

Adenine nucleotides and ventricular fibrillation.

The isolated perfused rat heart was used to study the influence of adenine nucleotides and their metabolites on vulnerability to ventricular fibrillation. In this model the incidence of ventricular arrhythmias after coronary artery ligation is determined by the extracellular K+ concentration; with perfusate K+ of 2.0 and 3.0 mmol/l hearts develop a high incidence of ventricular arrhythmias and fibrillation while arrhythmias are not encountered with perfusate K+ of 9.0 mmol/l. Assay of adenine nucleotides in uninvolved and ischaemic myocardium of these hearts showed a direct relationship between incidence of ventricular fibrillation and tissue levels of cyclic AMP but not tissue levels of lactate, high energy phosphates, adenosine, inosine and hypoxanthine/xanthine. Administration of dibutyryl cyclic AMP to isolated rat hearts reduced the ventricular fibrillation threshold; this action of cyclic AMP was effectively antagonized by adenosine and its N-ethylcarboxamido analogue but not by 2-chloroadenosine, phenylisopropyladenosine, cyclohexyladenosine and the adenosine deaminase inhibitor, EHNA. 2-Chloroadenosine, like adenosine, inhibited the increase in heart rate caused by DBcAMP. All the adenosine analogues had antiarrhythmic activity against spontaneously occurring ventricular arrhythmias during coronary artery occlusion. Adenosine analogues also antagonized the effect of dibutyryl cyclic AMP whereby it prolongs the QT interval. Adenosine, by as yet incompletely defined mechanisms, may act as an antagonist to the cyclic AMP mediated increase in vulnerability which contributes to the genesis of ventricular fibrillation in the early phase of myocardial ischaemia.

Adenine Nucleotides↗

PubMed1988

Prospective evaluation of a discriminant function for prediction of recurrent symptomatic ventricular tachycardia or ventricular fibrillation in coronary artery disease patients receiving amiodarone and having inducible ventricular tachycardia at electrophysiologic study.

Induction of ventricular tachycardia (VT) at electrophysiologic study in patients taking amiodarone poorly predicts recurrence of VT. Consequently, a discriminant function was developed (using parameters based on retrospective data) that appeared to identify high-risk patients. These parameters included ventricular effective refractory period, corrected QT interval, initiation of a repetitive ventricular response and the mode of VT induction. In the present study these parameters were prospectively evaluated in 60 patients with coronary artery disease and sustained VT or ventricular fibrillation (VF), in whom VT was still induced at electrophysiologic study during amiodarone therapy. Thirteen patients had recurrent events (sudden death in 8 and sustained VT in 5) and 47 patients had no symptomatic arrhythmia recurrence (follow-up for 16 +/- 2 months, mean +/- standard error of the mean). The ventricular effective refractory period, corrected QT interval and presence of a repetitive ventricular response did not discriminate between patients with and without symptomatic arrhythmia recurrence. However, an easier mode of VT induction during amiodarone therapy versus control was highly predictive of arrhythmia recurrence: 9 of 13 (69%) recurrences were in this group. In contrast, only 4 of 44 (9%) patients who had either the same or harder mode of VT induction had a recurrent event. Overall, 9 of 16 (56%) patients with an easier mode of VT induction had a recurrence, including 6 of the 8 patients with subsequent sudden cardiac death. It is concluded that electrophysiologic testing during amiodarone therapy is useful to identify high-risk patients.

Administration, Oral↗

PubMed1996

Effects of hypothyroidism on the vulnerability to ventricular fibrillation in dogs: a comparative study with amiodarone.

It has been shown that thyroid hormone has a significant effect on the heart and that suppression of thyroid function may contribute to the antiarrhythmic effect of amiodarone. The study was aimed at investigating the effects of hypothyroidism, compared with those of amiodarone, on vulnerability to ventricular fibrillation in dogs. In this study, 25 adult dogs were randomly divided into three groups: a hypothyroid group following total thyroidectomy (n = 9), an amiodarone group (n = 8, 400 mg per day, 4 weeks), and a control group (n = 8). Both amiodarone and control groups were subjected to sham surgery. Five to 8 weeks after surgery, ventricular fibrillation threshold and other electrophysiological parameters were determined. Right ventricular effective refractory period, monophasic action potential duration, and ventricular fibrillation threshold were significantly increased in both the thyroidectomized and amiodarone-treated animals. There was no significant change in monophasic action potential duration dispersion. The incidence of ventricular fibrillation during ischemia and reperfusion was significantly reduced in both treated groups compared with the sham-operated euthyroid controls. These observations suggest that hypothyroidism has a significant antifibrillatory effect in dogs. Homogeneous prolongation of repolarization and refractoriness may contribute to the antifibrillatory action of hypothyroidism.

Action Potentials↗

PubMed1990

Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation.

One hundred ninety-nine patients with out-of-hospital cardiac arrest persisted in ventricular fibrillation after the first defibrillation attempt and were then randomly assigned to receive either epinephrine or lidocaine before the next two shocks. The resulting electrocardiographic rhythms and outcomes for each group of patients were compared for each group and also compared with results during the prior 2 years, a period when similar patients primarily received sodium bicarbonate as initial adjunctive therapy. Asystole occurred after defibrillation with threefold frequency after repeated injection of lidocaine (15 of 59, 25%) compared with patients treated with epinephrine (four of 55, 7%) (p less than 0.02). There was no difference in the proportion of patients resuscitated after treatment with either lidocaine or epinephrine (51 of 106, 48% vs. 50 of 93, 54%) and in the proportion surviving (18, 19% vs. 21, 20%), respectively. Resuscitation (64% vs. 50%, p less than 0.005) but not survival rates (24% vs. 20%) were higher during the prior 2-year period in which initial adjunctive drug treatment for persistent ventricular fibrillation primarily consisted of a continuous infusion of sodium bicarbonate. The negative effect of lidocaine or epinephrine treatment was explained in part by their influence on delaying subsequent defibrillation attempts. Survival rates were highest (30%) in a subset of patients who received no drug therapy between shocks. We conclude that currently recommended doses of epinephrine and lidocaine are not useful for improving outcome in patients who persist in ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Bicarbonates↗

PubMed1990

Significance of discordant ST alternans in ventricular fibrillation.

With the use of epicardial mapping, we investigated the electrical alternans of the ST segment during acute myocardial ischemia and studied the difference in ST alternans between dogs with resultant ventricular fibrillation and those without it. During the 7-minute occlusion of the left anterior descending coronary artery below its first diagonal branch, 60 epicardial unipolar electrograms were recorded simultaneously at 1-minute intervals by a computerized mapping system. ST alternans was found in the eight dogs we observed. The amplitude of ST alternans (difference in the ST segment elevation of two consecutive electrograms) was greater in dogs with ventricular fibrillation (n = 4) than in those without it (n = 4) (3.92 +/- 1.24 versus 0.58 +/- 0.49 mV, p less than 0.05). Three of the four dogs with ventricular fibrillation demonstrated discordant ST alternans (i.e., adjacent leads were out of phase). Results from the present study indicate that an increased amplitude and discordance of ST alternans during acute myocardial ischemia are related to ventricular fibrillation and act as indicators of time and spatial unevenness of ventricular repolarization.

Animals↗

PubMed1981

Clinical efficacy and electrophysiology during long-term therapy for recurrent ventricular tachycardia or ventricular fibrillation.

We evaluated the effects of amiodarone in 45 patients with recurrent ventricular tachycardia or ventricular fibrillation. At a mean follow-up time of 12.7 +/- 8.8 months (range, three to 36), amiodarone was successful in nine of 16 patients with recurrent ventricular fibrillation and 21 of 29 with recurrent ventricular tachycardia. During amiodarone therapy, ventricular tachycardia could be induced in 18 of 19 patients in whom it had been induced before therapy, but only six of these 19 had spontaneous recurrence during follow-up. Side effects included corneal microdeposits, hyperthyroidism, blue skin, nausea, and symptomatic bradycardia. Pulmonary fibrosis occurred in three patients. Doses of up to 2000 mg a day did not produce cardiac toxicity, but neurologic side effects precluded long-term therapy at this dose. We conclude that amiodarone is effective for long-term therapy of recurrent ventricular tachyarrhythmias, that induction of arrhythmia during therapy does not always predict efficacy, and that side effects are frequent but do not usually limit therapy.

Adult↗

PubMed1976

Diabetic treatment and primary ventricular fibrillation in acute myocardial infarction.

The relation between mode of therapy and mortality rate and incidence of primary ventricular fibrillation was studied in 265 patients with diabetes mellitus and acute myocardial infarction. Sixty patients were being treated with diet only, 54 were receiving insulin and 151 were taking oral hypoglycemic agents. Fourteen patients (5.3 percent) had primary ventricular fibrillation, and all but one died. No statistically significant association was found between the incidence of primary ventricular fibrillation and the type of treatment for diabetes mellitus. Sixty-four (24.2 percent) of the 265 patients died during hospitalization. Mortality was greater among diabetic patients receiving oral therapy. However, after adjusting for age and sex, the difference among these three treatment regimens did not reach the P less than 0.05 level of significance.

Age Factors↗

PubMed1995

Dispersion of 'refractoriness' in noninfarcted myocardium of patients with ventricular tachycardia or ventricular fibrillation after myocardial infarction.

BACKGROUND: Postinfarction ventricular tachycardias (VTs) may degenerate into ventricular fibrillation (VF), but this does not happen in all patients. The underlying mechanism is not exactly known, but dispersion of refractory periods is considered a major factor in both induction and persistence of reentrant arrhythmias in general. Hypertrophied, noninfarcted myocardium has altered electrophysiological characteristics. We hypothesized that noninfarcted ventricular tissue may provide the heterogeneities that cause the transition from VT into VF. Local fibrillation intervals, ie, the average interval between local activations during VF, have previously been shown to correlate well with local refractoriness in human and canine atrium and in porcine and canine ventricle and may therefore be used as an index of local refractoriness. This technique permits simultaneous assessment of refractoriness at multiple sites. METHODS AND RESULTS: We measured local fibrillation intervals at 32 to 64 sites in the noninfarcted part of the left ventricle in patients undergoing antiarrhythmic surgery for symptomatic, drug-refractory, postinfarction ventricular tachyarrhythmias. The grid of electrodes (interelectrode distance, 7 mm) was attached to the epicardium of the left ventricle remote from the infarcted tissue. Group 1 consisted of 7 patients with hemodynamically tolerable sustained VT (VT group). Group 2 consisted of 7 patients with cardiac arrest and documented VF (VF group). With the patients on cardiopulmonary bypass, VF was induced by multiple premature stimulation. The VF interval was not significantly different in the two study groups (VT group, 136 +/- 5.5 ms; VF group, 129 +/- 3.4 ms, mean +/- SEM). However, spatial dispersion of the VF intervals (remote from the infarcted area) expressed as the coefficient of variation of VF intervals (SD x 100/mean VF interval in each heart) was significantly larger in the VF group. It was 3.63 +/- 0.56 in the VF group and 1.55 +/- 0.40 in the VT group (mean +/- SEM; P < .01). Differences between the shortest and longest VF intervals in one and the same heart and the largest difference between two adjacent sites were also larger in the VF group (P < .02 and P < .05, respectively). CONCLUSIONS: This study shows larger dispersion in VF intervals and therefore suggests larger dispersion of refractory periods in parts of the myocardium remote from the infarction in patients with postinfarction VF than in patients with postinfarction VT.

Aged↗

PubMed1985

Enhanced incidence of isoproterenol-induced ventricular fibrillation in the magnesium-deficient rat.

The electrocardiogram was recorded and serum and bulk myocardial electrolytes were determined in male Sprague Dawley rats, subjected to dietary magnesium deficiency for various periods, to assess the time course of development and cessation of the enhanced arrhythmogenic action of isoproterenol (150 micrograms/kg, subcutaneously) and to establish possible relationships between electrolyte changes and severe ventricular dysrhythmias. Ventricular fibrillation occurred within 60 min following isoproterenol injection in 25, 25, 62.5, 50, and 62.5% of rats on magnesium deficient diet for 4, 7, 11, 15, and 19 days (N = 8), respectively, and resulted in death in most animals (83%). Reintroduction of normal chow following a 30-day period on magnesium-deficient diet normalized serum magnesium (from 1.42 +/- 0.23 to 1.90 +/- 0.08 mEq/liter, mean +/- SD) but did not significantly reduce the incidence of ventricular fibrillation. Magnesium deficiency did not produce statistically significant alterations in bulk myocardial content of sodium, potassium, magnesium, and calcium. However, sodium was elevated and potassium diminished in hearts from rats that died in ventricular fibrillation, but not in those that had recovered. Magnesium-deficient rats sacrificed 30 min after isoproterenol injection, that is before the occurrence of ventricular fibrillation, exhibited hypomagnesemia and hypokalemia as well as elevated sodium and diminished potassium and magnesium in the myocardium. In contrast, rats on Purina Chow exhibited hypermagnesemia, but also showed hypokalemia and diminished cardiac potassium. The results indicate that magnesium deficiency enhances the arrhythmogenic propensity of isoproterenol and that the development of ventricular fibrillation is preceded by serum and myocardial electrolyte alterations.

Animals↗

PubMed2000

[Ventricular fibrillation in chronic heart disease].

The objective of the work was to describe in subjects with spontaneous ventricular fibrillation, after elimination of acute cardiac disease, the strategy of antiarrhythmic treatment and to evaluate, based on prospective follow-up, the effectiveness of this treatment. The authors included in the group 36 patients (30 men and 6 women) within the range from 34 to 78 years (mean age 58 +/- 11 years) with spontaneous ventricular fibrillation. They divided the group into a subgroup (15 subjects) without revascularization of the heart muscle, into a subgroup (17 subjects) with revascularization of the myocardium (coronary angioplasty and bypasses) and a subgroup (4 subjects) where ischaemic heart disease was ruled out (mostly cardiomyopathies). In all subgroups they used programmed ventricular stimulation (apparatuses of Quinton Co. USA, Biotronik Co. GFR), in the subgroup with revascularization within 3 months. During the diagnostic procedure of ventricular stimulation they tested antiarrhythmic drugs most frequently amiodarone per os (for 4 weeks). An implantable cardioverter--defibrillator was implanted in 17 patients (8 subjects without revascularization, 6 subjects with revascularization, 3 subjects without ischaemic heart disease). All patients were followed up till death, maximum 24 months. The authors evaluated the rate of cardiac deaths (death on cardiac grounds, incl. sudden arrhythmic death) and sudden arrhythmic deaths (within one hour after the onset of symptoms or the first malignant ventricular tachyarrhythmia recorded after implantation of the defibrillator). In the subgroup without revascularization with electric instability of the ventricles according to programmed stimulation 66.7% they described seven cardiac deaths (46.7%) and 6 sudden "arrhythmic" deaths (40%) incl. 5 subjects with ineffective testing of antiarrhythmic drugs. Conversely in the subgroup with revascularization and with diagnostic programmed stimulation in 47.1% they found 3 cardiac deaths (17.7%), one sudden "arrhythmic" death (5.9%)--a subject with ineffective testing. In the subgroup without ischaemic heart disease they recorded cardiac and sudden "arrhythmic" deaths in half the subjects, in all instances in subjects without inducible ventricular tachyarrhythmia. The authors found in the course of a two-year investigation a relapse of cardiac arrest in 25% of subjects after spontaneous ventricular fibrillation. A third of these subjects (all without a cardioverter-defibrillator) died. They confirm the benefit of implantation of a defibrillator for all subjects regardless of the basic diagnosis and revascularization of the heart muscle.

Adult↗

PubMed1991

Simultaneous right ventricular contraction and left ventricular fibrillation during cardiopulmonary bypass.

Two cases of brief left ventricular fibrillation concurrent with a beating right ventricle during cardiopulmonary bypass are described. Although no left or right ventricular dysfunction was detected postoperatively, this regional electrical heterogenicity suggests inhomogeneous myocardial protection during at least a short period of time. The precise mechanisms concerned are not clear and limited clinical and animal experimental analogies can be found in the literature.

Cardiopulmonary Bypass↗