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PubMed1984

Late induction of tachycardia in patients with ventricular fibrillation associated with acute myocardial infarction.

A prospective study was made of 57 asymptomatic patients, 1 to 24 months after acute myocardial infarction, 17 with (Group I) and 40 without (Group II) ventricular fibrillation during the acute event. None of the 57 patients had symptomatic arrhythmias, uncontrolled heart failure or unstable angina. There was no significant difference between the two patient groups in time from acute myocardial infarction, medication used or left ventricular ejection fraction. Repetitive forms of arrhythmia (Lown grade 4) were more prevalent (29 versus 16%, not significant) during 24 hour ambulatory monitoring in patients in Group I (ventricular fibrillation group). Programmed extrastimulation was performed using 1 to 3 twice-threshold, 2 ms decremental extrastimuli delivered during right ventricular drive. Of the 17 patients in Group I, 8 had no induced arrhythmia (less than or equal to 4 extra responses), 4 had nonsustained ventricular tachycardia and 5 had sustained ventricular tachycardia (degenerating into ventricular fibrillation requiring electrical reversion in 4). None of the 40 patients in Group II had induced sustained ventricular tachycardia (p less than 0.005), although 9 had nonsustained ventricular tachycardia. Patients with ventricular fibrillation during acute myocardial infarction may have an increased risk for ventricular tachycardia or ventricular fibrillation that may be exposed by programmed electrical stimulation even when not yet clinically manifest.

Adult↗

PubMed1995

Favourable outcome in idiopathic ventricular fibrillation with treatment aimed at prevention of high sympathetic tone and suppression of inducible arrhythmias.

OBJECTIVE: In the absence of an obvious cause for cardiac arrest, patients with idiopathic ventricular fibrillation are difficult to manage. A subset of patients has inducible arrhythmias. In others sympathetic excitation plays a role in the onset of the cardiac arrest. This study evaluates a prospective stepped care approach in the management of idiopathic ventricular fibrillation, with therapy first directed at induced arrhythmias and secondly at adrenergic trigger events. SETTING: University Hospital. PATIENTS: 10 consecutive patients successfully resuscitated from idiopathic ventricular fibrillation. INTERVENTIONS: Programmed electrical stimulation to determine inducibility, followed by serial drug treatment. Assessment of pre-arrest physical activity and mental stress status by interview, followed by beta blockade. Cardioverter-defibrillator implantation in non-inducible patients not showing significant arrest related sympathetic excitation. MAIN OUTCOME MEASURE: Recurrent cardiac arrest or ventricular tachycardia. RESULTS: Five patients were managed with serial drug treatment and four with beta blockade. In one patient a defibrillator was implanted. During a median follow up of 2.8 years (range 6 to 112 months) no patient died or experienced defibrillator shocks. One patient had a recurrence of a well tolerated ventricular tachycardia on disopyramide. CONCLUSIONS: Idiopathic ventricular fibrillation may be related to enhanced sympathetic activation. Prognosis may be favourable irrespective of the method of treatment. Whether the present approach enhances prognosis of idiopathic ventricular fibrillation remains to be determined. However, it may help to avoid potentially hazardous antiarrhythmic drugs or obviate the need for implantation of cardioverter-defibrillators.

Adult↗

PubMed1981

Extra-adrenergic mechanisms responsible for the effects of glucose-insulin-potassium solution on vulnerability to ventricular fibrillation.

In 53 chloralose-anesthetized dogs, the actions of glucose (10 mg/kg per min), insulin (0.025 U/kg per min) and potassium (0.025 mEq/kg per min) on the ventricular fibrillation and repetitive extrasystole thresholds were examined. Measurements were initially made in the control state and then repeated at 30, 60 and 120 minutes of infusion of glucose-insulin-potassium solution at a constant rate of 1.23 ml/min. The dogs received on the average 36 g of glucose, 44 U of insulin and 44 mEq of potassium over a 2 hour period. In the nonischemic myocardium, the infusion raised the threshold for ventricular fibrillation and repetitive extrasystole to a peak of 94 and 61 percent, respectively, without significantly changing serum potassium or circulating catecholamine concentration. In the ischemic myocardium, the incidence of spontaneous ventricular fibrillation during 10 minutes of coronary occlusion was reduced from 83 percent in the control state to 17 percent with glucose-insulin-potassium infusion. However, the infusion did not alter the incidence of ventricular fibrillation associated with reperfusion. Because cardio-cardiac sympathetic reflexes are elicited in response to coronary occlusion, the effect of glucose-insulin-potassium infusion on ventricular vulnerability during left stellate ganglion stimulation and norepinephrine infusion was investigated. The infusion completely prevented the reduction in the vulnerable period threshold during stellate stimulation and norepinephrine infusion. Furthermore, the peak protection afforded by the infusion was greater than that achieved with beta adrenergic blockade and was still present in catecholamine-depleted hearts. It is concluded that infusion of glucose-insulin-potassium solution protects against ventricular fibrillation in the normal and ischemic canine heart but not during reperfusion. This protection may be due in part to antagonism of adrenergic activity; however, the primary influence of the solution is mediated by extra-adrenergic mechanism.

Animals↗

PubMed1988

Ventricular fibrillation in acute experimental myocardial ischemia: protection by magnesium sulfate.

1. The efficacy of magnesium sulfate for prevention of ventricular fibrillation was compared with that of the calcium blocker verapamil and other antiarrhythmic drugs in 54 open-chested anesthetized dogs during a 3-h ligation of the circumflex coronary artery. Latency time to fibrillation, incidence of fibrillation and hemodynamic parameters were assessed. 2. Ventricular fibrillation occurred in 11 of 14 (79%) control dogs, in 2 of 8 (25%) dogs treated with magnesium sulfate (100 mg/kg) and in none of 8 animals treated with verapamil (0.2 mg/kg) (P = 0.014 and P = 0.0004, respectively, in comparison with controls); lidocaine (60 mg followed by 4 mg/min), amiodarone (5 mg/kg) and propafenone (4 mg/kg) had no effect on the incidence of fibrillation. 3. The latency time to fibrillation was 11.6 +/- 9.1 min in controls and it was shortened to 4.0 +/- 3.8 min (P = 0.039) in dogs treated with propafenone, but was unaffected by other drugs. 4. There was no correlation between pre-occlusion heart rate or blood pressure and fibrillation incidence. 5. In this experimental model, magnesium sulfate infusion had a protective effect against ventricular fibrillation that was similar to verapamil, suggesting that magnesium sulfate may be useful as an antifibrillatory agent during acute ischemia.

Analysis of Variance↗

PubMed1995

Diltiazem does not increase ventricular fibrillation threshold during hypothermia.

This study was designed to investigate whether the calcium channel blocker diltiazem affects the threshold for ventricular fibrillation during hypothermia in dogs. Ten dogs were cooled from 37 to 25 degrees C and rewarmed to 37 degrees C. The threshold for ventricular fibrillation was determined at body temperatures 37, 34, 31, 28 and 25 degrees C by programmed electrical stimulation using a stimulation protocol which involved application of maximal five extrastimuli. At 25 degrees C, six dogs were given an i.v. bolus dose of 100 micrograms.kg-1 followed by a continuous infusion of 100 micrograms.kg-1.h-1 of diltiazem hydrochloride. The other four dogs, were given no drugs at 25 degrees C and served as a control group. The dogs were rewarmed, and the stimulus protocol was performed at the same temperatures as during cooling. Cooling from 37 to 25 degrees C reduced the threshold for ventricular fibrillation in both groups. Heart rate were reduced, monophasic action potential duration at the apex and base of the heart increased from 167 +/- 5 ms to 469 +/- 17 ms and from 164 +/- 5 ms to 466 +/- 17 ms, respectively, when the temperature was reduced. The ventricular effective refractory period increased from 176 +/- 9 ms at 37 degrees C to 472 +/- 15 ms at 25 degrees C. Cooling increased QRS time on the ECG from 55 +/- 4 ms to 138 +/- 13 ms. Addition of diltiazem at 25 degrees C did not affect the threshold for ventricular fibrillation during rewarming. Further, diltiazem at 25 degrees C did not affect the heart rate or refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1988

The frequency of 'occult' ventricular fibrillation masquerading as a flat line in prehospital cardiac arrest.

We investigated the frequency with which a "vector of ventricular fibrillation" may exist in persons in prehospital cardiac arrest. Emergency medical technicians trained in defibrillation were directed to record the rhythm in three different monitor leads whenever they noted an initial flat line. Before these lead switches, the technicians performed a flat line protocol that included inspection of the lead connections to the patient and to the defibrillator, and checks of the calibration and battery status of the devices. They performed this flat line protocol for 127 cardiac arrest patients; 118 were in confirmed asystole after technical problems were corrected. Ventricular fibrillation was detected in only three (2.5%) when the monitor lead was switched. Initial technical problems were more frequent and were identified for ten patients (8%). The frequency of occult ventricular fibrillation (three of 118 asystolic patients) yields a 95% confidence that the true frequency is no greater than 8% to 9%. This suggests that ventricular fibrillation masquerading as asystole is rare. These data do not support protocols for empiric countershocks of patients with an initial flat line on the monitor.

Diagnosis, Differential↗

PubMed1989

Failure of amiodarone to prevent ventricular fibrillation (sudden death) in hypertrophic cardiomyopathy.

A case of ventricular fibrillation with successful resuscitation is described in a patient with hypertrophic cardiomyopathy and a history of syncope. Patients with hypertrophic cardiomyopathy who are at risk for sudden death can be identified by electrocardiographic monitoring which demonstrates episodes of ventricular tachycardia. Therapy with amiodarone has been shown to abolish ventricular tachycardia and to reduce the incidence of sudden death. Amiodarone therapy eliminated malignant ventricular ectopic activity in this patient during 48 h of ambulatory electrocardiographic monitoring, yet the subsequent exercise stress test provoked an episode of ventricular fibrillation.

Adult↗

PubMed1994

Initiation of ventricular fibrillation by atrial fibrillation.

We report the case of a patient who developed spontaneously a ventricular fibrillation during atrial fibrillation, 8 min after a perfusion of isoproterenol was stopped. Two mechanisms could explain the ventricular arrhythmia: silent ischaemia and a long-short cycle sequence just before ventricular fibrillation.

Atrial Fibrillation↗

PubMed1985

Lidocaine and prevention of ventricular fibrillation complicating acute myocardial infarction.

Prehospital prevention of primary ventricular fibrillation using 400 mg lidocaine i.m. may be effective in subjects aged under 70, but routine administration is not yet recommended since mortality was unaffected. Although in-hospital prevention of ventricular fibrillation can be achieved by routine i.v. administration of lidocaine in rather high dosages, this regimen is still controversial in well-equipped CCUs in view of conflicting results on mortality.

Aged↗

PubMed1983

Decreased vulnerability to ventricular fibrillation by vasodilator-induced baroreceptor sensitisation.

Vulnerability to ventricular fibrillation (VF) is affected by changes in systemic arterial blood pressure which are mediated through the sympathetic nervous system. We determined that small doses of a vasodilator drug can abolish the enhanced ventricular vulnerability induced by norepinephrine infusion. Noradrenaline (0.5 micrograms X kg-1 X min-1) caused a fall in ventricular fibrillation threshold from 30 to 20 mA (P less than 0.001). Pretreatment with prostaglandin E1, I2 or nitroglycerin at doses which reduced mean arterial blood pressure by 0.7 to 1.3 kPa (5 to 10 mmHg) abolished the enhanced vulnerability produced by noradrenaline. Following baroreceptor denervation, these agents no longer afforded protection against the profibrillatory action of noradrenaline. We conclude that small doses of vasodilator agents can augment ventricular electrical stability. The mechanism for this protective action appears to be a decrease in cardiac sympathetic tone resulting from vasodilatation of baroreceptor areas.

Alprostadil↗

PubMed1994

Aminophylline fails to improve the outcome of cardiopulmonary resuscitation from prolonged ventricular fibrillation: a placebo-controlled, randomized, blinded experimental study.

OBJECTIVES: The purpose of this study was to evaluate systematically the effects of the adenosine antagonist aminophylline on resuscitation outcome in a canine model of postcardioversion nonperfusing rhythm. BACKGROUND: Theoretic considerations and experimental studies indicate that myocardial adenosine accumulation during prolonged ventricular fibrillation might play a significant role in postcardioversion asystole and electromechanical dissociation. A recent uncontrolled clinical trial has suggested that the adenosine antagonist aminophylline might improve the outcome of cardiopulmonary resuscitation from refractory bradyasystolic cardiac arrest. METHODS: Two placebo-controlled, randomized, blinded experimental studies were performed. In protocol 1 (20 dogs), ventricular fibrillation was induced and maintained for 7.5 min. Sixty seconds before cardioversion, dogs received 1 mg of epinephrine followed by 250 mg of aminophylline or placebo. In protocol 2 (20 dogs), dogs were cardioverted to electromechanical dissociation after 5 min of unsupported ventricular fibrillation. Sixty seconds later, all dogs received 1 mg of epinephrine followed by 250 mg of aminophylline or placebo. In both experiments, resuscitation efforts were continued until return of spontaneous circulation, or up to 30 min. The primary end point was survival to 1 h. RESULTS: In protocol 1, 4 of 10 dogs survived in the aminophylline group, whereas 7 of 10 dogs survived in the placebo group, a nonsignificant trend toward unfavorable outcome from aminophylline. Pretreatment with aminophylline increased the number of cardioversion applications required to terminate ventricular fibrillation. In protocol 2, 5 of 10 and 6 of 10 dogs survived in the aminophylline and placebo groups, respectively. CONCLUSIONS: The results of this study suggest that aminophylline fails to improve the outcome of resuscitation from prolonged ventricular fibrillation. It does not reverse established electromechanical dissociation and may in fact increase the number of cardioversion applications required to terminate ventricular fibrillation. The rationale for conducting clinical trials with aminophylline during cardiopulmonary resuscitation is questionable.

Aminophylline↗

PubMed1978

Surgical division of an accessory atrioventricular connection in the posterior septal region following ventricular fibrillation in the Wolff-Parkinson-White syndrome.

A young man presented with atrial fibrillation and a rapid ventricular response which degenerated into ventricular fibrillation. Electrophysiological study demonstrated an accessory atrioventricular connection in the posterior septal region. This was sectioned to prevent recurrence of his arrhythmia. Post-operative electrophysiological study demonstrated that the surgical section was successful.

Adolescent↗

PubMed1976

Effects of unilateral cardiac sympathetic denervation on the ventricular fibrillation threshold.

A train of gated stimuli scanning the entire vulnerable period was delivered to the right anterior or left posterior ventricular surface to study the ventricular fibrillation threshold in anesthetized and vagotomized dogs. Heart rate was held constant by atrial pacing. Measurements were obtained in control conditions and after surgical removal of one stellate ganglion. To avoid the shortcomings associated with an irreversible procedure like stellectomy, control fibrillation threshold measurements were also alternated with determinations during reversible blockade by cooling of one stellate ganglion. The results were similar with both techniques. In nine animals, ablation or cooling of the left stellate ganglion increased ventricular fibrillation threshold by 72 +/- 35 (mean +/- standard deviation) percent compared with control values (P less than 0.001). By contrast, in 11 animals, ablation or cooling of the right stellate ganglion lowered the threshold by 48 +/- 14 percent compared with control values (P less than 0.001). Electrode location did not influence the results. The observed changes depended solely upon unilateral removal of cardiac sympathetic activity and were not demonstrable if such activity was low. These results suggest that right and left cardiac sympathetic nerves may have different and specific effects on cardiac excitability. They also contribute to the understanding of the pathogenesis of the long Q-T syndrome (characterized by episodes of ventricular fibrillation associated with increased sympathetic activity) and increase the rationale for left stellectomy as the specific treatment for this illness. Left stellectomy, by raising the ventricular fibrillation threshold, may also represent an alternative measure in patients at high risk of sudden death from ventricular arrhythmias resistant to medical therapy.

Animals↗

PubMed1979

Prophylaxis of ventricular fibrillation after acute experimental coronary occlusion by chronic beta-adrenoceptor blockade with atenolol.

Acute occlusions of the left circumflex coronary artery were performed in open-chest dogs. A control group (n = 19) was compared with three groups (total n = 17) pretreated once daily with different doses of the cardioselective beta-blocking drug atenolol (ICI 66 082) given by mouth for 5 days. Only animals without coronary collateral vessels were examined, having a mortality rate of 100% in the control group. Arrhythmias and ventricular fibrillation during the first 30 min after coronary occlusion showed a biphasic distribution in time (phase 1a and 1b). A lower degree of beta-adrenoceptor blockade reduced the incidence of arrhythmias and ventricular fibrillation in phase 1a, but fibrillation occurred in all animals during phase 1b. A higher dose of the beta-blocking drug protected the animals from ventricular fibrillation, and arrhythmias in phase 1a were greatly reduced. At all times the ventricular fibrillation threshold in the group pretreated with atenolol was significantly higher than in the control group. In both groups a significant decrease in ventricular fibrillation threshold was found only during phase 1a. The greater sensitivity of phase 1a arrhythmias to beta-blockade and the lack of a decrease in ventricular fibrillation threshold during phase 1b might indicate differences in the genesis of arrhythmias and fibrillation in phases 1a and 1b.

Animals↗

PubMed1997

Tedisamil increases coherence during ventricular fibrillation and decreases defibrillation energy requirements.

INTRODUCTION: Drugs which primarily prolong cardiac refractoriness decrease defibrillation voltage and energy requirements in animals and man. The effect of such drugs on ventricular fibrillation itself is not well understood. We hypothesized that tedisamil, an investigational antiarrhythmic drug which blocks Ito and IK repolarizing potassium channels, would increase organization of epicardial electrograms during ventricular fibrillation while it lowered defibrillation energy requirements. METHODS: We measured magnitude-squared coherence, a measure of spatial organization, and ventricular fibrillation (VF) cycle length, ventricular effective refractory period (VERP), and monophasic action potential duration (APD90) as well as defibrillation energy threshold (E50) at baseline and after 150 micrograms/kg of tedisamil (n = 13) or saline control (n = 6) in an open chest dog model. RESULTS: After tedisamil, mean magnitude-squared coherence increased by 132 +/- 133%, from 0.15 +/- 0.08 to 0.31 +/- 0.16 (P < 0.001); VF cycle length increased from 121 +/- 24 to 190 +/- 63 ms (P < 0.001) and became more regular, with the coefficient of variation between adjacent VF intervals decreasing from 14.1 +/- 6.9 to 3.9 +/- 2.2% (P < 0.001). Mean E50 decreased from 8.9 +/- 3.8 to 6.1 +/- 2.7 joules (P < 0.001); VERP increased from 158 +/- 30 to 201 +/- 31 ms (P < 0.001), and APD90 increased from 177 +/- 25 to 244 +/- 45 ms (P < 0.001) after tedisamil. No electrophysiologic parameter was changed after saline infusion. CONCLUSIONS: Tedisamil increases both spatial coherence and temporal regularity of ventricular fibrillation. These effects on 'order' during VF may be in part responsible for the observed reduction in defibrillation energy requirements.

Animals↗

PubMed1994

Changes in arterial and mixed venous blood gases during untreated ventricular fibrillation and cardiopulmonary resuscitation.

This investigation was designed to evaluate the changes in arterial and mixed venous acid-base conditions during untreated ventricular fibrillation and after institution of cardiopulmonary resuscitation (CPR). Fifty-two swine (weight: 25-40 kg) were studied after induction of ventricular fibrillation. In a subgroup of 10 animals, 10-min CPR trials were performed. Arterial and mixed venous blood gases were monitored at baseline, after 5 min of untreated ventricular fibrillation (nonintervention interval) and after 10 min of mechanical CPR. Standard CPR was performed at compression rates of 100/min with a 60% duty cycle. Arterial pH, Pco2, and HCO3 were unchanged when baseline values were compared with those obtained after 5 min of untreated ventricular fibrillation, while arterial Po2 decreased from 81 to 69 torr. Mixed venous pH decreased from 7.41 to 7.35, Pco2 increased from 43 to 48 torr, Po2 decreased from 40 to 38 torr and HCO3 decreased from 28 to 26 mEq/l (P < 0.05). Although these changes were statistically significant, many remain in the normal range. Both arterial and mixed venous pH and HCO3 fell further after 9 min of CPR and Pco2 increased (P < 0.05). Alterations in mixed venous pH and Pco2 were more apparent than corresponding changes in arterial blood gas composition. We conclude that untreated cardiac arrest may be accompanied by normal arterial and mixed venous blood gas levels. Tissue acidosis is only revealed after tissue perfusion is restored and is most accurately reflected in the mixed venous blood gas composition. This apparent paradox provides insight into the relationship between tissue perfusion and arterial and mixed venous acid-based composition.

Acid-Base Equilibrium↗

PubMedDate not supplied

Maintenance of circulation during ventricular fibrillation with the simultaneous use of two "counterpulsation" devices.

Two valveless, single orifice counterpulsation devices, with pumping stroke volumes of 65 ml each, were implanted on the ascending aorta and pulmonary artery of seven open chest anesthetized dogs. After completion of the preparation, ventricular fibrillation was induced. The devices were synchronized to pump simultaneously at a rate of 85-100 bpm. The combined use of the counterpulsation devices provided maximal aortic pressure of 111.4 +/- 25.1 mmHg during ventricular fibrillation for a period of 15-60 min. The mean left ventricular pressure was 17.7 +/- 4.4 mmHg, and the cardiac index 64.5 +/- 23.6 ml/kg/min. Cardioversion of ventricular fibrillation to sinus rhythm restored normal hemodynamics. The counterpulsation device implanted on the ascending aorta was not able to maintain circulation for more than 5 min after the induction of ventricular fibrillation, if used alone. In conclusion, the use of two counterpulsation devices implanted on the ascending aorta and pulmonary artery was able to maintain circulation in experimental animals during ventricular fibrillation.

Animals↗

PubMed2003

[Brugada syndrome associated with ventricular fibrillation induced by administration of pilsicainide: a case report].

A 56-year-old man with Brugada syndrome presented with ventricular fibrillation induced by administration of pilsicainide. He had syncope at age 46 years, and his uncle suddenly died of unknown cause. He had taken pilsicainide (150 mg/day) for paroxysmal atrial fibrillation, and suffered from syncope due to ventricular fibrillation. Coved type ST elevation was observed in the V1 lead, and saddle back type ST elevation was observed in the V2 lead. The ST elevation gradually recovered after stopping pilsicainide therapy. No structural heart disease was found. After intravenous injection of pilsicainide, the ST segment elevated in the V1 and V2 leads. Ventricular fibrillation was induced by triple extrastimulation at the right ventricular apex. The diagnosis was Brugada syndrome, and a cardioverter-defibrillator was implanted. Brugada syndrome should be considered before administering pilsicainide.

Anti-Arrhythmia Agents↗