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PubMed1999

Coherence between body surface ECG leads and intracardiac signals increases during the first 10 s of ventricular fibrillation in the human heart.

Ventricular fibrillation (VF) in the human heart is not well understood. The aim of this study was to measure changes in the phase relationship between the body surface ECG and intracardiac electrograms recorded during the first 10 s of human VF. We studied 11 episodes of VF and measured the coherence of (a) ECG lead I and ECG lead V1, (b) ECG lead V1 and the right ventricular apex (RVA) electrogram, and (c) ECG lead V1 and the smoothed RVA electrogram. Each coherence measurement was the average of the magnitude squared coherence function in the range 0-60 Hz, and measurements were made 1, 3, 5, 7 and 9 s after the onset of VF. Overall, the mean (SD) coherence was 31(6)% between ECG leads I and V1, 17(3)% between ECG lead V1 and the RVA electrogram, and 20(4)% between ECG lead V1 and the smoothed RVA electrogram. All three measurements of coherence increased significantly between 1 and 9 s with mean (SD) rates of 0.97(1.01)% s(-1), 0.8(1.18)% s(-1) and 0.82(1.19)% s(-1) respectively. These results show that propagation in human VF becomes more organized during the first 10 s of VF. This may be an optimal window for defibrillation.

Cardiac Catheterization↗
PubMed1982

Reduction of ventricular fibrillation threshold by histamine: resolution into separate H1- and H2-mediated components.

The effects of histamine and the selective agonists impromidine (H2-agonist) and 2-(2-thiazolyl ethylamine)(H1-agonist) on ventricular fibrillation threshold were tested in the isolated guinea-pig heart. All three compounds produced reversible concentration-dependent decreases in ventricular fibrillation threshold. Ventricular fibrillation threshold reduction was not secondary to the positive chronotropic effect of the three compounds. Computer analysis of the data using appropriate theoretical models suggests that the net effect of histamine on ventricular fibrillation threshold is the resultant of two components: H1 and H2. Pyrilamine inhibited the H1-mediated effects of histamine on ventricular fibrillation threshold with a Kb value of 0.449 nM. H1- and H2-receptors mediating ventricular fibrillation threshold reduction differ in their relative sensitivity to histamine (H1 greater than H2; EC50 for histamine, 53.9 nM at H1- and 311 nM at H2-receptors) and in the maximum response which they are capable of producing (H1 congruent to 1/2 that of H2). The finding that extremely low concentrations of histamine (less than 1 pg/ml) can effectively reduce ventricular fibrillation threshold reinforces the concept that histamine is highly arrhythmogenic.

Animals↗
PubMed1981

The effects of thioridazine on electrical and ischemic ventricular fibrillation in the dog heart in situ.

Lethal ventricular arrhythmias have occurred in patients taking thioridazine. Therefore, we studied two canine models to determine if thioridazine alters vulnerability to ventricular fibrillation. In 30 chloralose-anesthetized dogs, the repetitive response threshold was used to assess vulnerability during right ventricular stimulation with transvenous catheter electrodes. Placebo, 10 mg/kg of thioridazine (therapeutic dose) or 30 mg/kg of thioridazine (high dose) was infused i.v. (n = 10 each group). Repetitive response threshold, diastolic excitability, QRS, Q-Tc and plasma thioridazine concentrations were measured before and after drug. Both 10 and 30 mg/kg of thioridazine increased diastolic excitability threshold (P < .05) while only the 30 mg/kg dose widened QRS (P < .05) and prolonged Q-Tc (P < .05). RRT was unchanged. In 45 pentobarbital-anesthetized dogs, one stage ligation of the left anterior descending coronary artery was performed after pretreatment with placebo, 10 or 30 mg/kg of thioridazine (n = 15 each group). Spontaneous ventricular fibrillation occurred in 6 of 15 dogs (40%) after placebo, 8 of 15 dogs (53%) after 10 mg/kg of thioridazine and 14 of 15 dogs (93%) after 30 mg/ kg of thioridazine. Although thioridazine depressed excitability and had no effect on electrical fibrillation threshold, the 30 mg/kg dose increased the likelihood of spontaneous ventricular fibrillation during acute ischemia.

Animals↗
PubMed1981

Relation between conduction delay and ventricular fibrillation: characteristics of conduction of premature impulses during acute myocardial ischemia.

Critical conduction delay has been shown to be the important factor in reentrant arrhythmias. To determine the causal relation between conduction delay and spontaneous ischemic ventricular fibrillation, conduction delay of induced premature ventricular impulses in the ischemic and the border zones of ventricular myocardium was investigated in 23 dogs. There were 8 control dogs, 9 dogs that manifested ventricular fibrillation within 30 minutes of ligation of the distal left anterior descending coronary artery (group I), and 6 dogs that manifested ventricular fibrillation between 30 and 60 minutes of ligation of the proximal left anterior descending coronary artery (group II). Conduction delay was measured as the change of conduction time from preligation levels to postligation levels in epicardial and endocardial sites in both base to apex (anterograde) and apex to base (retrograde) directions. Conduction delay in all four directions was compared in the control group and groups I and II (ventricular fibrillation). By means of continuous recordings on tape, the origin of ventricular fibrillation was determined to be in the ischemic zone (13 of 15 dogs) or in the border zone (2 of 15 dogs). Conduction delay in all directions was greater in the group with ventricular fibrillation whether the fibrillation occurred after the first or second ligation. Specifically, epicardial anterograde conduction (in the border zone) and retrograde conduction (in the ischemic zone) were significantly delayed in group I. Conduction in group II was significantly delayed in both the ischemic and the border zones in three of four directions at 35 minutes. The rate of change of conduction time in all four directions was significantly greater in the group with ventricular fibrillation than in the control group. Pending further work, this model may provide a reliable marker for the development of spontaneous ventricular fibrillation during acute myocardial ischemia and may permit assessment of various interventions as specific therapy for acute reentrant ischemic tachyarrhythmias leading to ventricular fibrillation.

Acute Disease↗
PubMed1988

Clinical characteristics of patients with ventricular fibrillation during antiarrhythmic drug therapy.

We retrospectively studied 28 patients with 38 episodes of newly occurring ventricular fibrillation during antiarrhythmic drug therapy. Twenty-six of these patients, who had ventricular fibrillation during single-drug therapy with quinidine, procainamide, or disopyramide, were compared with a control group of 62 patients who had been treated similarly for ventricular arrhythmias but did not have ventricular fibrillation during treatment. The median duration of therapy before ventricular fibrillation was three days. The left ventricular ejection fraction of the study group was lower than that of the control group (0.29 vs. 0.43; P less than 0.0001), and concomitant treatment with digitalis and diuretic agents was more common in the study group. The base-line QT interval (corrected for heart rate) was slightly longer in the study group than in the controls (0.47 vs. 0.44; P less than 0.005), although both groups had similar degrees of QT prolongation during drug therapy. Four of 13 patients (31 percent) who underwent multiple trials of antiarrhythmic drugs had recurrent episodes of ventricular fibrillation. Six patients died suddenly after a mean follow-up of 18 months--four who were receiving antiarrhythmic therapy and two who were not. We conclude that drug-associated ventricular fibrillation is an early event, that there may be an increased risk of its recurrence with subsequent trials of antiarrhythmic drugs, and that left ventricular dysfunction and concomitant therapy with digitalis and diuretic agents may predispose patients to this complication.

Anti-Arrhythmia Agents↗
PubMed1998

Changes in human coronary sinus blood flow and myocardial metabolism induced by ventricular fibrillation and defibrillation.

BACKGROUND: During implantation of cardioverter-defibrillators, repeated inductions of ventricular fibrillation and defibrillation are performed. Little is known about the myocardial metabolism associated with ventricular fibrillation and defibrillation in humans. METHODS: Sixteen patients scheduled for transvenous cardioverter-defibrillator implantation were included in the study. In 10 of the patients, blood samples were taken simultaneously in the coronary sinus and radial artery and analyzed for PO2, PCO2, standard bicarbonate, pH, lactate, alanine, glucose, and glycerol. Oxygen saturation, base excess, and oxygen content were calculated. The patients were studied before, shortly after, and 2 and 5 minutes after successful defibrillation. In six of the patients, coronary sinus blood flow was registered continuously. RESULTS: The coronary sinus blood flow declined from a basal value of 93 +/- 16 mL/min to 35 +/- 6 mL/min 14 +/- 2 seconds after induction of ventricular fibrillation. Following termination of ventricular fibrillation, coronary sinus blood flow increased to a peak value of 227 +/- 75 mL/min. Oxygen saturation, PO2, and oxygen content in the coronary sinus increased by approximately 25% shortly after each episode of ventricular fibrillation and defibrillation. The coronary sinus lactate increased and the arterio-coronary sinus lactate difference decreased shortly after each of the four episodes, but was normalized within 2 minutes. CONCLUSIONS: Repeated threshold tests during defibrillator implantation did not cause any long-lasting or cumulative metabolic effects, indicating that the described technique, with a 5-minute recovery period in between episodes, is safe as regards myocardial metabolism.

Adult↗
PubMed1989

Electrophysiologic actions and antifibrillatory efficacy of subacute left stellectomy in a conscious, post-infarction canine model of ischemic ventricular fibrillation.

The autonomic nervous system appears to modulate ventricular arrhythmias associated with acute myocardial ischemia. This study investigated the electrophysiologic effects and antifibrillatory actions of subacute left stellectomy in a conscious, post-infarction canine model of sudden cardiac death. Twenty-two dogs with a previous anterior wall myocardial infarction and inducible ventricular arrhythmias were randomized to undergo either left stellectomy (n = 12) or remain as sham-denervated controls (n = 10). Five to 7 days post left stellectomy, there were no significant changes in heart rate, electrocardiographic intervals or ventricular refractoriness compared to sham-denervated controls. Acute posterolateral ischemia was produced in left stellectomy and sham-denervated dogs by anodal current-induced thrombosis via a previously positioned electrode in the left circumflex coronary artery. Ventricular fibrillation developed within 1 hour of the onset of ischemia (early ventricular fibrillation) in 3/12 (25%) left stellectomy dogs versus 8/10 (80%) sham-denervated controls (P less than 0.05). However, 24-hour mortality rate was 5/12 (42%) after left stellectomy versus 8/10 (80%) after sham denervation (P = 0.072). Small differences in regional myocardial norepinephrine content, which is a marker for neuronal integrity, occurred in the mid-posterolateral and mid-anteroseptal regions of the left ventricle after left stellectomy. Overall norepinephrine concentration after left stellectomy was 409.70 +/- 9.90 ng/g vs 428.07 +/- 10.84 ng/g in sham controls (P = NS). In summary, subacute left stellectomy significantly reduces the incidence of ventricular fibrillation occurring within 1 hour of the onset of acute posterolateral ischemia at a distance to a previous myocardial infarction in conscious dogs, and tends to reduce the ischemic post-infarction mortality at 24 hours after the onset of ischemia. This protective effect of left stellectomy is not due to any alteration in cardiac electrophysiologic parameters measured prior to the development of acute posterolateral ischemia, nor is it related to regional denervation as determined by myocardial tissue concentration of residual norepinephrine.

Animals↗
PubMed2003

The effects of nifedipine on ventricular fibrillation mean frequency in a porcine model of prolonged cardiopulmonary resuscitation.

UNLABELLED: We assessed the effects of a calcium channel blocker versus saline placebo on ventricular fibrillation mean frequency and hemodynamic variables during prolonged cardiopulmonary resuscitation (CPR). Before cardiac arrest, 10 animals were randomly assigned to receive either nifedipine (0.64 mg/kg; n = 5) or saline placebo (n = 5) over 10 min. Immediately after drug administration, ventricular fibrillation was induced. After 4 min of cardiac arrest and 18 min of basic life support CPR, defibrillation was attempted. Ninety seconds after the induction of cardiac arrest, ventricular fibrillation mean frequency was significantly (P < 0.01) increased in nifedipine versus placebo pigs (mean +/- SD: 12.4 +/- 2.1 Hz versus 8 +/- 0.7 Hz). From 2 to 18.5 min after the induction of cardiac arrest, no differences in ventricular fibrillation mean frequency were detected between groups. Before defibrillation, ventricular fibrillation mean frequency was significantly (P < 0.05) increased in nifedipine versus placebo animals (9.7 +/- 1.2 Hz versus 7.1 +/- 1.3 Hz). Coronary perfusion pressure was significantly lower in the nifedipine than in the placebo group from the induction of ventricular fibrillation to 11.5 min of cardiac arrest; no animal had a return of spontaneous circulation after defibrillation. In conclusion, nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR; this was nevertheless associated with no defibrillation success. IMPLICATIONS: This study evaluates the effects of a calcium channel blocker on ventricular fibrillation mean frequency, hemodynamic variables, and resuscitability during prolonged cardiopulmonary resuscitation (CPR) in pigs. Nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR but did not improve resuscitability.

Animals↗
PubMed1989

Effects of pretreatment with propranolol on potassium, calcium, and magnesium shifts after ventricular fibrillation in dogs.

Hypokalemia and other electrolyte changes have been observed after resuscitation from ventricular fibrillation. We studied the effect of propranolol on postresuscitation electrolytes in a canine model of ventricular fibrillation and cardiac resuscitation by randomizing 40 anesthetized dogs to four groups: ventricular fibrillation--no drug (VF), ventricular fibrillation--propranolol pretreatment (VF-prop), control-no drug (NoVF), control--propranolol (NoVF-prop). We measured serum electrolytes at baseline and periodically for 3 hours. In VF dogs, serum potassium decreased from 3.9 +/- 0.4 to 3.2 +/- 0.2 mEq/L 60 minutes after resuscitation (p less than 0.001). The decrease in potassium was prevented (p less than 0.001) by propranolol. Serum calcium decreased from 10.6 +/- 0.8 to 10.2 +/- 0.8 mg/dl in VF dogs 15 minutes after resuscitation (p less than 0.05); this decrease was not blocked by propranolol (p = NS). Serum magnesium increased from 1.5 +/- 0.2 to 1.8 +/- 0.1 mEq/L in VF dogs 7 minutes after resuscitation (p less than 0.001); this rise was partially blocked by propranolol (p less than 0.01). Serum glucose increased from 105 +/- 6 to 183 +/- 27 mg/dl in VF dogs 7 minutes after resuscitation (p less than 0.001); this increase was diminished by propranolol (p less than 0.001). Thus propranolol prevents the decrease in serum potassium after ventricular fibrillation in this canine model, providing evidence that postresuscitation hypokalemia is caused by the beta-adrenergic effects of catecholamines secreted in response to cardiac arrest. Propranolol blocks the rise in magnesium and glucose but does not block the decrease in calcium after resuscitation.

Animals↗
PubMed1987

Spontaneous termination of prolonged ventricular fibrillation after acute myocardial infarction.

We describe a case of ventricular fibrillation occurring during acute myocardial infarction converting to sinus rhythm without specific additional drug therapy or direct current cardioversion. Ventricular fibrillation occurred during therapy with a temporary transvenous bipolar pacemaker and prophylactic intravenous lidocaine. Reversion of ventricular fibrillation without direct current cardioversion is unusual. Direct current shock remains the first form of treatment for witnessed ventricular fibrillation.

Aged↗
PubMed1976

Cyclic AMP as a determinant of vulnerability to ventricular fibrillation in the isolated rat heart.

Ventricular fibrillation threshold and vulnerable period were measured in the isolated perfused rat heart to assess the influence of dibutyryl cyclic AMP on ventricular vulnerability. Doses of dibutyryl cyclic AMP of 0.6-1.6 mumol/min caused an increase in coronary flow but had no effect on vulnerability, whereas doses of 2.6-4.2 mumol/min resulted in an increase in coronary flow, a decrease in VF threshold, and an increase in the width of the vulnerable period. These experiments support the concept of a local myocardial action of catecholamines, mediated by cyclic AMP, whereby vulnerability to ventricular fibrillation is increased.

Animals↗
PubMed2006

[Ventricular fibrillation in a patient with three accessory pathways, Ebstein anomaly and intermittent long QT interval. RF ablation and electrophysiologic considerations].

We present a case of a 19-year old man with minor Ebstein's anomaly, intermittent long QT interval and WPW syndrome in whom atrial fibrillation, degenerating into ventricular fibrillation was the first symptom. QRS complex morphologies during atrial fibrillation revealed the presence of three accessory pathways (septal, right inferior paraseptal and antero-inferior). Immediately after resuscitation the patient was treated with amiodarone, which resulted in a significant prolongation of QT interval to 700 ms. After RF ablation of accessory pathways patient remains asymptomatic during 6-month follow up, however QTc interval is about 500 ms.

Adult↗
PubMed1994

Idiopathic ventricular fibrillation in out-of-hospital cardiac arrest survivors.

This study examined diagnostic and therapeutic roles of electrophysiological testing and long-term clinical outcome after out-of-hospital cardiac arrest due to idiopathic ventricular fibrillation. This is defined as ventricular fibrillation occurring in the absence of detectable underlying heart disease or metabolic or electrolyte disturbance. Out-of-hospital cardiac arrest resulting from idiopathic ventricular fibrillation is uncommon. Records of all patients who underwent electrophysiological testing between June 1979 and June 1992 were reviewed. Patients with out-of-hospital cardiac arrest due to idiopathic ventricular fibrillation were identified. Follow-up information was obtained by telephone interview in June 1992. Of 194 patients who underwent electrophysiological study after out-of-hospital cardiac arrest not associated with acute myocardial infarction, only six (4 male and 2 female) had idiopathic ventricular fibrillation. It was induced in only two patients by programmed ventricular stimulation. No sustained ventricular arrhythmias were induced in the remaining four patients. Four patients received implantable cardioverter defibrillators, one was treated with a beta-adrenergic blocker, and one received no treatment. All patients were alive at a mean follow-up of 50 months. Two of the four patients without inducible sustained ventricular arrhythmias had events during follow-up. Of the two patients with inducible ventricular fibrillation, one experienced a cardiac arrest and documented ventricular fibrillation at 41 months after the index event and the other had had no recurrence at 15-month follow-up. All four patients with implantable cardioverter defibrillators were alive at last follow-up, and two had device discharges.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[Conditions facilitating the development of secondary ventricular fibrillation].

The relationship between left-ventricular end diastolic pressure (Pllv) and size (llv) in secondary ventricular fibrillation was investigated in 28 diseased cardiac patients. A critical level is identified in the Pllv:llv ratio at the time of secondary ventricular fibrillation, that is assumed to precondition this kind of arrhythmia. The demonstrated relationship is similar to the relation of atrial fibrillation to the critical balance achieved between the respective left-atrial parameters.

Adolescent↗
PubMed1979

Ventricular fibrillation in the Wolff-Parkinson-White syndrome.

To examine the risk of ventricular fibrillation in patients with the Wolff-Parkinson-White syndrome, we compared patients who had this syndrome and a history of ventricular fibrillation related to preexcitation with patients who had the syndrome without this history. Ventricular fibrillation occurred during atrial fibrillation, with rapid conduction over the accessory pathway, and these patients had a higher prevalence of both reciprocating tachycardia and atrial fibrillation (14 of 25 vs. 18 of 73, P = 0.004) and multiple accessory pathways (five of 25 vs. four of 73, P = 0.012). The shortest preexcitation R-R interval during atrial fibrillation was less in the group with ventricular fibrillation (mean shortest R-R, 180 vs. 240 milliseconds, P less than 0.0001) as was the average R-R interval (mean average R-R, 269 vs 340 milliseconds, P less than 0.0001). Patients with Wolff-Parkinson-White syndrome who are most susceptible to ventricular fibrillation have a history of atrial fibrillation and reciprocating tachycardia, demonstrate rapid conduction over an accessory pathway during atrial fibrillation and have multiple accessory pathways.

Adolescent↗
PubMed1989

Low-osmolality contrast media-induced ventricular fibrillation.

We evaluated the incidence of ventricular fibrillation with low-osmolality contrast media by right coronary arteriography in eleven adult mongrel dogs. Following insertion of the catheter into the right coronary artery, a test solution was infused for 25 seconds (total 11 mL) or until fibrillation occurred. The test solutions included 20% mannitol, ioxaglate, iopamidol, iotrolan, and sodium iopamidol, which contained 150 mEq/L sodium in solution. The incidences of ventricular fibrillation were 0% with iotrolan, 8.3% with sodium iopamidol, 10% with ioxaglate, and 100% with iopamidol and mannitol. These observations suggest that the absence of sodium ions is a critical factor in fibrillation, even in low-osmolality contrast media. The fact that iotrolan had the least arrhythmogenic property may be attributed to the 8 mEq/L of sodium ions in that agent.

Animals↗
PubMed1993

Synergistic effects of haemodynamic stabilisation and beta blockade on ventricular fibrillation threshold in coronary artery ligated pigs.

OBJECTIVE: The aim was (1) to test the hypothesis that the prevention of haemodynamic deterioration decreases arrhythmia formation in the infarcting heart and augments the antiarrhythmic effects of beta blockade; and (2) to assess the ventricular fibrillation threshold as an index of innate arrhythmogenic propensity. METHODS: Changes in ventricular fibrillation threshold as an index of innate arrhythmogenic propensity. METHODS: Changes in ventricular fibrillation threshold were determined for 50 min after anterior descending coronary artery occlusion in open chest pigs (group 1, n = 5). In group 2 (n = 9), ventricular fibrillation threshold was studied in the same way but cardiac output was maintained at 100 ml.min-1.kg-1 body weight and mean aortic pressure at 60(SEM 3) mm Hg by means of right heart and arterio-arterial bypass. In both groups intravenous propranolol 1.2 mg.kg-1 was injected 35-40 min after coronary artery occlusion. In group 3 (n = 6) spontaneous arrhythmias following coronary artery occlusion were recorded to test how well the ventricular fibrillation threshold reflected the incidence and time course of these arrhythmias. RESULTS: In group 1, there was a deep trough in ventricular fibrillation threshold--from 11.3(0.3) mA to 6.0(0.3) mA--within 10 min of coronary artery occlusion (47% decrease, p < 0.001). There was a shallower trough between 10 and 30 min. In group 2, preocclusion ventricular fibrillation threshold increased from 13.9(1.2) mA to 32.1(5.6) mA (p < 0.05) because of stabilised haemodynamics. After coronary occlusion, fibrillation threshold remained high throughout, being 22.7(1.3) mA and 20.4(1.1) mA at the times of the expected troughs (p < 0.005 v group 1 for both values). Propranolol increased ventricular fibrillation threshold by 24(7)% in group 1 (p < 0.05) and by 53(8)% in group 2 (p < 0.0005). In group 3 spontaneous arrhythmias followed a biphasic pattern, similar to group 1. There was a positive correlation between ventricular fibrillation threshold and arrhythmia score (r = 0.84). CONCLUSIONS: (1) Haemodynamic stabilisation increased ventricular fibrillation threshold during ischaemia and enhanced the antiarrhythmic effects of beta blockade. (2) The ventricular fibrillation threshold accurately reflects the incidence and time course of spontaneous arrhythmias in this model.

Adrenergic beta-Antagonists↗