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PubMed1989

Randomized study of epinephrine versus methoxamine in prehospital ventricular fibrillation.

Experimental data suggest that a pure alpha-agonist, such as methoxamine, may improve the outcome of patients in ventricular fibrillation. A double-blind, randomized, prospective study was conducted in a paramedic system comparing the use of methoxamine with epinephrine in enhancing conversion of ventricular fibrillation while otherwise following American Heart Association protocols. One hundred two patients in ventricular fibrillation not responding to initial defibrillations with a pulsatile rhythm were randomized into one of two groups, each containing 51 patients. Equipressor doses of epinephrine (0.5 mg) and methoxamine (5 mg) were given intravenously and repeated according to American Heart Association guidelines. The mean age, sex ratio, and mean paramedic response times were comparable for the two groups. The mean time at scene until conversion was 22 +/- 10 minutes for methoxamine and 17 +/- 7 minutes for epinephrine (P = NS). The methoxamine group received 3.1 +/- 1.4 doses as compared with 2.8 +/- 1.3 doses for the epinephrine group (P = NS). Conversion rate, defined as the percentage of patients who developed a pulse during resuscitation, was 27.5% for the methoxamine group and 49.0% for the epinephrine group (P less than or equal to .03). Successful resuscitation, defined as the conveyance of a patient to an emergency department with a pulse and rhythm, was 17.7% for the methoxamine group and 39.2% for the epinephrine group (P less than or equal to .02). Save rate, defined as the percentage of patients discharged alive after hospitalization, was 7.8% for the methoxamine group and 19.6% for the epinephrine group (P less than or equal to .07).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1975

Effects of aminophylline on the threshold for initiating ventricular fibrillation during respiratory failure.

Cardiac arrhythmias have frequently been reported in association with respiratory failure. The possible additive role of pharmacologic agents in precipitating cardiac disturbances in patients with respiratory failure has only recently been emphasized. The effects of aminophylline on the ventricular fibrillation threshold during normal acid-base conditions and during respiratory failure were studied in anesthetized open chest dogs. The ventricular fibrillation threshold was measured by passing a gated train of 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. During the infusion of aminophylline, the ventricular fibrillation threshold was reduced by 30 to 40 percent of the control when pH and partial pressures of oxygen (PO2) and carbon dioxide (CO2) were kept within normal limits. When respiratory failure was produced by hypoventilation (pH 7.05 to 7.25; PC02 70 to 100 mm Hg: P02 20 to 40 mm Hg), infusion of aminophylline resulted in an even greater decrease in ventricular fibrillation threshold to 60 percent of the control level. These experiments suggest that although many factors may contribute to the increased incidence of ventricular arrhythmias in respiratory failure, pharmacologic agents, particularly aminophylline, may play a significant role.

Acid-Base Equilibrium↗
PubMed1992

Effect of BN 52256 and other mediator antagonists on ouabain-induced ventricular fibrillation in sensitized guinea-pigs and on ischemia-induced fibrillation in rats.

The threshold dose of ouabain necessary to induce ventricular fibrillation is decreased in sensitized guinea-pigs signalizing an enhanced arrhythmogenicity. Esculetine or WEB 2170 antagonists of histamine and PAF, respectively and especially a combination of both can increase the threshold dose of ouabain-induced fibrillation demonstrating an antiarrhythmic effect. BN 52256 a substance with multi-antagonistic properties shows antiarrhythmic effect in this method, too. WEB 2170 and BN 52256 decrease the incidence of ventricular fibrillation after coronary ligation in rats.

Anesthesia↗
PubMed1978

Efficacy of lidocaine in preventing primary ventricular fibrillation within 1 hour after a 300 mg intramuscular injection. A double-blind, randomized study of 300 hospitalized patients with acute myocardial infarction.

The effectiveness of intramuscular lidocaine in preventing in-hospital primary ventricular fibrillation within 1 hour after injection of the drug in patients with acute myocardial infarction was assessed in a double-blind randomized study performed in 300 such patients admitted within 6 hours of myocardial infarction. Six of 147 patients treated with 300 mg of intamuscular lidocaine had ventricular fibrillation compared with 4 of 153 control subjects. The lidocaine blood level of the patients who experienced ventricular fibrillation was 1.4 +/- 0.7 microgram/ml (mean +/- standard deviation) at the time of fibrillation, a value not significantly different from that of treated patients who did not experience fibrillation. Lidocaine blood levels in the latter were 1.9 +/- 1.1, 2.1 +/- 1.1, 2.1 +/- 1.1 and 1.7 +/- 0.7 microgram/ml, respectively, 7, 15, 30 and 60 minutes after injection. In this study intramuscular lidocaine was ineffective in preventing ventricular fibrillation, possibly because the given dose, 300 mg, prevented attainment of adequqte blood levels of the drug.

Adult↗
PubMed1997

The association between blood lactate concentration on admission, duration of cardiac arrest, and functional neurological recovery in patients resuscitated from ventricular fibrillation.

OBJECTIVE: To assess the association between arterial lactate concentration on admission and the duration of human ventricular fibrillation cardiac arrest, and to what degree the arterial lactate concentration on admission is an early predictor of functional neurological recovery in human cardiac arrest survivors. DESIGN: Cohort study. Arterial lactate concentrations and out-of-hospital data concerning cardiac arrest and cardiopulmonary resuscitation were collected retrospectively according to a standardized protocol. Functional neurological recovery was assessed prospectively at regular intervals for 6 months. SETTING: Emergency department of an urban tertiary care hospital. PATIENTS: A total of 167 primary survivors of witnessed out-of-hospital ventricular fibrillation cardiac arrest. MEASUREMENTS: The association between arterial lactate concentration on admission, the duration of cardiac arrest, and functional neurological recovery was assessed. Further, we assessed whether admission concentrations of arterial lactate and duration of cardiac arrest can predict unfavorable functional neurological recovery. Functional neurological recovery was measured in cerebral performance categories (CPC). No or minimal functional impairment (CPC 1 and 2) was defined as favorable outcome; the remaining categories (CPC 3, 4 and 5) were defined as unfavorable functional neurological recovery. RESULTS: In 167 patients, a weak association between total duration of cardiac arrest and admission levels of lactate (r = 0.49, P < 0.001) could be shown. With increasing admission concentrations of arterial lactate functional neurological recovery was more likely to be unfavorable (OR 1.15 per mmol/l increase, 95% CI 1.04-1.27). Nevertheless, only at very high levels of lactate (16.3 mmol/l) could unfavorable neurological recovery be detected with 100% specificity, yielding a very low sensitivity of 16%. CONCLUSIONS: The arterial admission lactate concentration after out-of-hospital ventricular fibrillation cardiac arrest is a weak measure of the duration of ischemia. High admission lactate levels are associated with severe neurological impairment. However, this parameter has poor prognostic value for individual estimation of the severity of subsequent functional neurological impairment.

Aged↗
PubMed1991

Effects of atrioventricular block on ventricular fibrillation threshold in dog.

The effects of complete atrioventricular block (CAVB) on ventricular vulnerability were studied 1 week after a transcatheter electrical ablation of the AV junction in 18 closed-chest dogs. All dogs exhibited CAVB and a stable ventricular escape rhythm with a mean cycle length of 1795 +/- 600 ms. Although QT interval during CAVB was significantly prolonged compared with that during the sinus rhythm, QTc interval was significantly shortened. The ventricular fibrillation threshold was significantly elevated after creation of the block (from 9.35 +/- 2.28 to 12.3 +/- 3.69 mA, p less than 0.01). Thus, CAVB which is not associated with QTc prolongation would be even less likely to play an important role in producing ventricular fibrillation presumably including torsades de pointes or polymorphous ventricular tachycardia.

Animals↗
PubMed1993

Circadian variation of sudden cardiac death reflects age-related variability in ventricular fibrillation.

BACKGROUND: Previous studies report a morning peak in the occurrence of out-of-hospital sudden cardiac death but lack detailed information on underlying arrhythmias. We used the documentation system of the semiautomated defibrillators used by emergency medical technicians to investigate the circadian pattern of defined arrhythmias and the influence of demographic patient characteristics on this pattern. METHODS AND RESULTS: From December 1988 to December 1990, 703 consecutive patients (63% men; age, 67 +/- 17 years) with sudden cardiac death were registered in the Klinikum Steglitz area of the Berlin emergency care system. Determination of time of day of the event was based on the arrival time of the rescue squad. A marked circadian variation (P < .0001) in the occurrence of sudden cardiac death was observed with a primary morning peak (6 AM to noon) and a secondary afternoon peak (3 to 7 PM). The subgroup of 294 patients with ventricular fibrillation as initially documented arrhythmia showed a similar circadian variation (P < .0001). In significant contrast (P < .01), patients with asystole (n = 260) or pulseless bradyarrhythmias (n = 149) were more evenly distributed during the daytime with a primary night trough. Multivariate logistic regression analysis revealed that the circadian pattern of ventricular fibrillation was similar in both gender groups but tended to differ with regard to age: patients older than 65 years demonstrated a monophasic distribution, whereas patients aged 65 years or less had a biphasic distribution with peaks in the morning and in the afternoon. CONCLUSIONS: The circadian pattern of sudden cardiac death reflects primarily a circadian variation in onset of ventricular fibrillation. The different circadian patterns of ventricular fibrillation, pulseless bradyarrhythmias, and asystole suggest different pathophysiological mechanisms of causation of death. The age dependence of the pattern of ventricular fibrillation may indicate different underlying external or endogenous triggers.

Adolescent↗
PubMed2004

Non-invasive evaluation of ventricular refractoriness and its dispersion during ventricular fibrillation in patients with implantable cardioverter defibrillator.

BACKGROUND: Local ventricular refractoriness and its dispersion during ventricular fibrillation (VF) have not been well evaluated, due to methodological difficulties. METHODS: In this study, a non-invasive method was used in evaluation of local ventricular refractoriness and its dispersion during induced VF in 11 patients with VF and/or polymorphic ventricular tachycardia (VT) who have implanted an implantable cardioverter defibrillator (ICD). Bipolar electrograms were simultaneously recorded from the lower oesophagus behind the posterior left ventricle (LV) via an oesophageal electrode and from the right ventricular (RV) apex via telemetry from the implanted ICD. VF intervals were used as an estimate of the ventricular effective refractory period (VERP). In 6 patients, VERP was also measured during sinus rhythm at the RV apex and outflow tract (RVOT) using conventional extra stimulus technique. RESULTS: Electrograms recorded from the RV apex and the lower esophagus behind the posterior LV manifested distinct differences of the local ventricular activities. The estimated VERPs during induced VF in the RV apex were significantly shorter than that measured during sinus rhythm using extra stimulus technique. The maximal dispersion of the estimated VERPs during induced VF between the RV apex and posterior LV was that of 10 percentile VF interval (40 +/- 27 ms), that is markedly greater than the previously reported dispersion of ventricular repolarization without malignant ventricular arrhythmias (30-36 ms). CONCLUSIONS: This study verified the feasibility of recording local ventricular activities via oesophageal electrode and via telemetry from an implanted ICD and the usefulness of VF intervals obtained using this non-invasive technique in evaluation of the dispersion of refractoriness in patients with ICD implantation.

Adult↗
PubMed1986

Ventricular fibrillation threshold in canine hearts with quinidine induced prolonged QT interval: effects of atrial pacing, isoproterenol, and lignocaine.

Ventricular fibrillation threshold was determined using a train of pulses, 4 ms in duration, delivered at 10 ms intervals, in 20 anaesthetised dogs receiving toxic doses of quinidine sulphate (30 mg X kg-1) injected intravenously over 5 min to prolong the QT interval. The effects of atrial pacing, isoproterenol, and lignocaine on ventricular fibrillation threshold were investigated. Quinidine administration lowered the mean(SD) threshold from 14.7(5.1) to 8.8(3.6) mA (n = 20, p less than 0.001). Atrial pacing shortened the mean(SD) basic cycle length from 652 to 400 ms and the QT interval (378(28) vs 334(19) ms, n = 8, p less than 0.01) but did not alter the mean(SD) threshold (7.0(2.3) vs 7.5(1.5) mA). Isoproterenol infusion to maintain basic cycle length at 421(23) ms shortened the mean(SD) QT interval to 291(14) ms (p less than 0.001) and increased the mean(SD) threshold to 13.6(5.9) mA (n = 8, p less than 0.01). Lignocaine (plasma concentration 1.36 micrograms X ml-1) increased the mean(SD) threshold from 10.9(3.4) to 16.7(6.7) mA (n = 7, p less than 0.02) without affecting basic cycle length and QT interval. Thus atrial pacing shortened the QT interval slightly but did not make the canine heart with a quinidine induced prolonged QT interval less vulnerable to electrically induced ventricular fibrillation, whereas both isoproterenol and lignocaine did, although they affected basic cycle length and QT interval differently.

Animals↗
PubMed1984

Prevention of ventricular fibrillation during acute myocardial infarction by intravenous propranolol.

A trial of intravenous followed by oral propranolol, started within 4 h of onset of suspected myocardial infarction and continued over 27 h, was carried out in 735 patients; 364 received propranolol, 371 were controls. Ventricular fibrillation during the first 48 h after entry to the trial occurred in 2 treated patients and in 14 controls (p = 0.006). Rates of hospital mortality, complications other than ventricular fibrillation, and progression from threatened to completed infarction did not differ between treated and control patients. Ventricular fibrillation was not apparently prevented by prior beta-blocker treatment, which was not a reason for exclusion from the trial. This intravenous/oral propranolol regimen seems to prevent ventricular fibrillation due to evolving myocardial infarction.

Administration, Oral↗
PubMed1985

Effect of aprindine, verapamil and nifedipine on ventricular fibrillation threshold in isolated rabbit hearts.

The effect of aprindine, verapamil and nifedipine on electrical stimulation threshold (EST) and ventricular fibrillation threshold (VFT) was studied in isolated rabbit hearts. Aprindine steeply raised EST and VFT in a dose-dependent manner. With the highest concentration of aprindine tested (0.56 mumol/l), protection against electrically-induced ventricular fibrillation was achieved in 4 out of 6 hearts after 60 min exposure to the drug. Perfusion with verapamil (0.1 and 0.2 mumol/l) and nifedipine (0.14 and 0.21 mumol/l) produced significant rise in both thresholds. When the hearts were perfused with higher concentration (0.3 mumol/l verapamil, 0.28 mumol/l nifedipine), EST and VFT did not continue to be increased in a dose-dependent manner but actually dropped below the control value in most hearts. These results suggest that the effect of aprindine on EST and VFT is different from that of verapamil and nifedipine and further indicate a limited effectiveness of these two slow channel blockers against ventricular fibrillation.

Animals↗
PubMed1977

The treatment of patients with recurrent ventricular fibrillation.

During the four year period from 1972 to 1975, eleven patients, eight with recurrent and three with first attacks of ventricular fibrillation, underwent aortocoronary bypass graft and/or resection of ventricular aneurysm. All patients had old myocardial infarction from seven weeks to six years. Left ventricular angiography demonstrated discrete aneurysm of the anterior wall of the left ventricle in nine of the patients and akinesis or hypokinesis of the anterior and posterior wall of the left ventricle in the remaining two. Coronary angiography was carried out in ten patients and revealed significant disease of the left anterior descending and right coronary arteries in ten and nine patients, respectively. There was no operative mortality, and there were two late deaths. Eight patients have improved significantly and have had no further sign of ventricular irritability. The present study indicates that aortocoronary bypass graft and/or resection of ventricular aneurysm is an effective method of therapy for patients with repeacted ventricular fibrillation who have ventricular aneurysm and ischemic heart disease.

Adult↗
PubMed1982

Supra spinal influence on ventricular fibrillation threshold and cardiac stores of norepinephrine in the cat.

The relationship between ventricular fibrillation threshold (VFT) as measured by voltage required to evoke ventricular fibrillation and the concentration of norepinephrine (NE) in different parts of the myocardium under experimental interventions has been studied in anaesthetized cats. A selective increase in VFT and a marked reduction in NE content have been observed after spinal transection, removal of spinal cord from cervical 6 to thoracic 6 or carotid sinus denervation. Reserpine pretreatment significantly reduces NE content of myocardium but fails to affect VFT. The fibrillating left ventricle shows a marked decline in NE content from the control level of 1.55 +/- 0.32 to 0.82 +/- 0.09 micrograms/g and there is also a similar concomitant reduction in NE content of the entire heart. Defibrillation brings back normal rhythm, but does not restore the NE content immediately. The results suggest that a marked reduction in cardiac stores of norepinephrine significantly affect VFT and that the central nervous system plays an important role in the genesis of sustained ventricular arrhythmia.

Animals↗
PubMed1984

Ventricular fibrillation and transient arrhythmias after defibrillation in patients with acute myocardial infarction.

Ventricular fibrillation (VF) and transient arrhythmias after defibrillation were analyzed from the recordings of 28 patients containing at least one episode of ventricular fibrillation. An R-on-T extrasystole initiated VF in 60% of the episodes. Other initiating factors were a late premature beat (24%), stable ventricular tachycardia (VT) (7%), accelerating idioventricular rhythm (5%) and cardioversion of VT (5%) with a sinusoidal waveform. After the initiating beat, in most cases, evidence was found of a transient ventricular tachycardia which then deteriorated into VF. With a stable VT this may occur after a long time; in the case of apolymorphic VT (with changing amplitude) it generally occurred within 30 s. The main transient arrhythmias generated by circulatory arrest during VF and by the defibrillation shock were: total arrest, total AV-block and/or bradycardia. The combination of a longer duration of VF and a high energy level generally resulted in an increase in the duration of these arrhythmias (P less than 0.01, N = 30). Comparison of episodes of VT and VF recorded in a single patient also shows that arrhythmias are more unfavourable and of longer duration after VF than after VT. These data emphasize fast defibrillation, initially with stored energy levels less than 250J.

Adult↗
PubMed1987

Effect of flecainide acetate on prevention of electrical induction of ventricular tachycardia and occurrence of ischemic ventricular fibrillation during the early postmyocardial infarction period: evaluation in a conscious canine model of sudden death.

The antiarrhythmic and antifibrillatory effects of flecainide acetate during the early postinfarction period were evaluated in a conscious canine model of sudden cardiac death. Ventricular tachycardia remained inducible early after infarction in eight of nine dogs receiving an intravenous loading dose of flecainide (2.0 mg/kg body weight) and seven of eight dogs receiving saline vehicle. In both the drug and vehicle groups, there was no significant change in the ventricular refractory period or in the cycle length of the induced ventricular tachycardia. With a maintenance intravenous infusion of flecainide, 1.0 mg/kg per h for 4 hours, the subsequent occurrence of acute posterolateral ischemia resulted in the development of ventricular fibrillation and sudden death in seven of eight flecainide-treated and eight of eight vehicle-treated dogs. Seven additional postinfarction dogs with noninducible tachycardia during pretreatment programmed stimulation, and thereby considered to be at "low risk" for the development of ischemic ventricular fibrillation, were also given flecainide in an intravenous loading and maintenance dosing regimen. The subsequent occurrence of posterolateral ischemia resulted in the development of ventricular fibrillation in three of these seven dogs. These findings suggest that flecainide acetate may not possess pharmacologic properties useful in managing ventricular tachycardia or in preventing ischemic ventricular fibrillation in the presence of recent myocardial damage.

Animals↗
PubMed2006

Evidence for multiple mechanisms in human ventricular fibrillation.

BACKGROUND: The mechanisms that sustain ventricular fibrillation (VF) in the human heart remain unclear. Experimental models have demonstrated either a periodic source (mother rotor) or multiple wavelets as the mechanism underlying VF. The aim of this study was to map electrical activity from the entire ventricular epicardium of human hearts to establish the relative roles of these mechanisms in sustaining early human VF. METHODS AND RESULTS: In 10 patients undergoing cardiac surgery, VF was induced by burst pacing, and 20 to 40 seconds of epicardial activity was sampled (1 kHz) with a sock containing 256 unipolar contact electrodes connected to a UnEmap system. Signals were interpolated from the electrode sites to a fine regular grid (100x100 points), and dominant frequencies (DFs) were calculated with a fast Fourier transform with a moving 4096-ms window (10-ms increments). Epicardial phase was calculated at each grid point with the Hilbert transform, and phase singularities and activation wavefronts were identified at 10-ms intervals. Early human VF was sustained by large coherent wavefronts punctuated by periods of disorganized wavelet behavior. The initial fitted DF intercept was 5.11 +/- 0.25 (mean +/- SE) Hz (P < 0.0001), and DF increased at a rate of 0.018 +/- 0.005 Hz/s (P < 0.01) during VF, whereas combinations of homogeneous, heterogeneous, static, and mobile DF domains were observed for each of the patients. Epicardial reentry was present in all fibrillating hearts, typically with low numbers of phase singularities. In some cases, persistent phase singularities interacted with multiple complex wavelets; in other cases, VF was driven at times by a single reentrant wave that swept the entire epicardium for several cycles. CONCLUSIONS: Our data support both the mother rotor and multiple wavelet mechanisms of VF, which do not appear to be mutually exclusive in the human heart.

Aged↗
PubMed1994

Dofetilide reduces the incidence of ventricular fibrillation during acute myocardial ischaemia. A randomised study in pigs.

OBJECTIVE: The aim was to investigate whether dofetilide, a new selective cardiac potassium channel blocker, would reduce the incidence of ischaemia induced ventricular fibrillation in closed chest pigs. METHODS: A randomised, blinded, and placebo controlled study was performed in 32 closed chest pigs with a body weight of 70-90 kg. The animals were given a dofetilide/placebo bolus of 25 micrograms.kg-1 over a 10 min period followed by a maintenance dose of 12.5 micrograms.kg-1.h-1 for the next 130 min. Electrocardiograms were recorded during sinus rhythm and during atrial pacing, before (t0) and 20 min (t20) after the beginning of drug treatment. Twenty minutes after the start of drug treatment, acute myocardial ischaemia was induced by inflation of a percutaneous transluminal coronary angioplasty (PTCA) balloon placed in the left anterior descending coronary artery proximal to the first diagonal branch. If ventricular fibrillation occurred during the 2 h ischaemia period the balloon was deflated and defibrillation attempted by dc shocks (360 joules) up to a maximum of 10 shocks. RESULTS: Basal characteristics for the dofetilide group (n = 16) and the placebo group (n = 16) were similar: body weight 76.1(SD 5.4) kg v 75.4(4.4) kg; heart weight 296(29) g v 302(43) g; and heart rate (RR interval) 854(261) ms v 800(307) ms. During atrial pacing 100 beats.min-1 the paced QT interval (QTp) measured at t0 in the dofetilide group and the placebo group were similar, at 335(36) ms v 330(31) ms, respectively. During drug treatment (t20) the QTp interval increased to 412(38) ms in the dofetilide group (p < 0.001) whereas a much smaller increase to 341(32) ms was observed in the placebo group (p < 0.05). The heart rate and ST elevation in the two groups were similar during coronary artery occlusion. During the 2 h ischaemic period, ventricular fibrillation occurred in 6/16 (38%) of the dofetilide treated pigs, and in 13/16 (81%) of the placebo treated pigs (p < 0.01). Defibrillation was successful in 5/6 (83%) and 6/13 (46%) of the animals, respectively (p = 0.3). CONCLUSIONS: Dofetilide significantly reduces the incidence of ischaemia induced ventricular fibrillation in closed chest pigs.

Animals↗