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PubMedDate not supplied

Changes in ventricular fibrillation threshold during acute hypothermia. A model for future studies.

Hypothermia and rewarming are associated with an increased incidence of lethal arrhythmias in man. The relationship between reduction in body temperature and ventricular fibrillation threshold was studied in 7 pentobarbital anaesthetized dogs using programmable electrical stimulation while cooling and rewarming between 37 degrees C and 25 degrees C in steps of 3 degrees C. Fibrillation threshold was defined as the number of extrastimuli required to evoke ventricular fibrillation. QRS-durations and corrected QT-intervals (QTc) were measured from surface electrocardiograms. Monophasic action potential durations were recorded from the base and apex of the heart. Fibrillation threshold decreased with decreasing temperatures; e.g., at 37 degrees C ventricular fibrillation was not inducible after 5 extrastimuli, while at 25 degrees C only 2 extrastimuli were required. From 37 degrees C to 25 degrees C QRS-width, monophasic action potential durations and QTc increased while conduction velocity decreased. The differential effects on conduction and monophasic action potential duration provide a basis for induction of ventricular fibrillation during acute hypothermia. This model of hypothermia-induced ventricular fibrillation should prove useful for future studies aimed at understanding the mechanisms responsible for hypothermia-related deaths.

Action Potentials↗
PubMed1998

Experimental studies of electroacupuncture on ventricular fibrillation threshold in rats with acute ischemic myocardium.

By ligating the proximate left anterior descend (LAD) of coronary artery and inducing the ventricular fibrillation with electrical stimulation, the preventive effects of electroacupuncture (EA) on ventricular fibrillation were observed. The results showed that the ventricular fibrillation threshold (VFT) of rats with acute ischemic myocardium was raised after acupuncturing some acupoints, which could prevent the occurrence of ventricular fibrillation. Furthermore, the combination of EA and propranolol could enhance the VFT effectively, and they showed a good synergistic effect.

Adrenergic beta-Antagonists↗
PubMed1989

Exercise training after experimental myocardial infarction increases the ventricular fibrillation threshold before and after the onset of reinfarction in the isolated rat heart.

Previous work has shown that exercise training increases the ventricular fibrillation threshold of the isolated perfused rat heart. The aim of our study was to determine whether exercise training that begins after myocardial infarction can similarly increase the ventricular fibrillation threshold. Rats that had suffered an experimental myocardial infarction were subject to a running training program. Thereafter, the ventricular fibrillation threshold was measured before and after the onset of acute reinfarction induced by a second coronary artery ligation. Ventricular fibrillation thresholds were significantly elevated in trained rats during normoxia (13.7 +/- 2.2 vs. 4.7 +/- 0.8 mA, p less than 0.01) and during acute ischemia (6.8 +/- 1.6 vs. 3.0 +/- 0.7 mA, p less than 0.02). The myocardial cyclic AMP level was lower in the nonischemic zone of the trained hearts (0.21 +/- 0.01 vs. 0.28 +/- 0.01 nmol/g, p less than 0.05), which also had lower cyclic AMP levels after epinephrine challenge (0.50 +/- 0.05 vs. 0.73 +/- 0.09 nmol/g, p less than 0.01; 1.41 +/- 0.11 vs. 1.85 +/- 0.09 nmol/g, p less than 0.02 after epinephrine 10(-7) M and 5 x 10(-6) M injection, trained vs. untrained). Both propranolol 10(-6) M and epinephrine 5 x 10(-7) M attenuated the difference in ventricular fibrillation thresholds before and after second coronary artery ligation and eliminated any difference in cyclic AMP content of both the nonischemic and ischemic myocardial tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Increased risk of ventricular fibrillation associated with temporary pacemaker use during coronary arteriography.

Each injection of angiographic contrast dye during coronary arteriography represents a "natural experiment" in which the human ventricular fibrillation threshold is transiently reduced. Few factors, however, have been identified which favor the actual occurrence of ventricular fibrillation in this setting. Of 3906 consecutive patients undergoing selective coronary arteriography with sodium meglumine diatrizoate, 66 (1.7 percent) experienced dye-induced ventricular fibrillation, from which all were successfully defibrillated. Analysis of these cases revealed, unexpectedly, that patients in whom temporary right ventricular pacemakers were employed had an incidence of ventricular fibrillation nearly six times that found in the entire group undergoing arteriography (10 percent vs. 1.7 percent, respectively; P less than .001). Those individuals receiving pacemakers were distinguished from other studied patients only by a higher prevalence of conduction abnormalities. Although there is normally a low probability that mechanical stimulation by a pacing catheter can induce ventricular fibrillation, it is postulated that such an occurrence may be more likely after ventricular vulnerability has been increased by contrast dye.

Adult↗
PubMed2003

Sodium-hydrogen exchange inhibition preserves ventricular function after ventricular fibrillation in the intact swine heart.

BACKGROUND: We tested the hypothesis that sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after ischemia-reperfusion injury in the intact porcine heart. METHODS: Twelve pigs (weight, 30-45 kg) were evenly divided into 2 groups. Baseline ventricular function studies were based on echocardiography, conductance, aortic flow, and left ventricular pressure. Animals were given vehicle (control) or benzamide-N-(aminoiminomethl)-4-(4-[2-furanylcarbonyl]-1-piperazinyl)-3-(methylsulfonyl)methanesulfonate (BIIB 513; 3 mg/kg administered intravenously). Ten minutes later, hearts were subjected to 75 seconds of ventricular fibrillation. After reperfusion for 40 minutes, function studies were repeated. Hearts were arrested and excised. Postmortem data included passive pressure-volume curves and myocardial water content. RESULTS: Preload recruitable stroke work was significantly decreased from baseline after ischemia and reperfusion in the control group (27.7 +/- 2.5 vs 48.0 +/- 5.6 mm Hg [+/- SEM], P =.001) but not in the BIIB 513 group (43.0 +/- 5.8 vs 45.5 +/- 4.1 mm Hg, P = not significant). In vivo diastolic and postmortem passive left ventricular compliance were reduced after ischemia and reperfusion for control animals but remained unchanged for animals receiving BIIB 513. Time required to recover baseline blood pressure after ventricular fibrillation was significantly longer for control animals (159 +/- 15 vs 88 +/- 14 seconds [+/- SEM], P =.008). Myocardial water content (78.97% +/- 0.94% vs 77.86% +/- 0.46% [+/- SEM]) and normalized left ventricular mass (137.24 +/- 6.17 vs 128.41 +/- 1.96 g [+/- SEM]) were insignificantly increased in control animals. CONCLUSIONS: Sodium-hydrogen exchange inhibition attenuates ventricular dysfunction after 75 seconds of ventricular fibrillation and 40 minutes of reperfusion. This family of agents might prove useful in patients with severe left ventricular dysfunction undergoing ventricular fibrillation for implantable cardioverter defibrillator testing.

Animals↗
PubMed1988

Initial treatment of ventricular fibrillation: defibrillation or drug therapy.

The belief that defibrillation of unwitnessed ventricular fibrillation frequently results in asystole, combined with perceived low survival rates, led to deviation from "standard" advanced cardiac life support (ACLS) by physicians directing paramedics in the field. In nonstandard ACLS, intubation or drug therapy preceded defibrillation. This study retrospectively compared standard and nonstandard ACLS for ventricular fibrillation. The long-term survival rates were 12.3% (7/57) and 3.6% (6/168) for the two forms of ACLS, respectively (p = 0.03). The incidence of postcountershock asystole was 35% and 28% (p = 0.45). The survival rates for patients with a postcountershock rhythm and a pulse were 83% and 17% after standard and nonstandard ACLS (p less than 0.0001). Other factors reported to have a significant effect on survival were compared, and no significant differences (p greater than 0.05) were noted for mean age, sex, cardiopulmonary resuscitation (CPR) initiated by a bystander, ACLS response time, time to CPR, lay-witnessed arrest, or time to definitive care. The significant difference in the time to defibrillation (14 and 26 minutes) was expected. This is the first clinical study to clearly confirm the ACLS recommendation of early defibrillation before drug therapy in ventricular fibrillation.

Aged↗
PubMed1975

Effects of xylazine and acetylpromazine upon induced ventricular fibrillation in dogs anesthetized with thiamylal and halothane.

Ventricular arryhythmias including ventricular fibrillation were produced with epinephrine in dogs induced to an anesthetic state with thiamylal and maintained with halothane. In dogs given (premedicated) xylazine 20 minutes prior to anesthesia, ventricular arrhythmias, including ventricular fibrillation, were induced with much smaller doses of epinephrine than in nonpremedicated dogs. Dogs premedicated with acetylpromazine 20 minutes prior to anesthesia with thiamylal and halothane displayed protection from epinephrine-induced arrhythmias. Caution is advised from using xylazine in the presence of halothane if epinephrine is to be administered.

Anesthesia↗
PubMed2001

Algorithms to analyze ventricular fibrillation signals.

Prediction of the success of defibrillation to avoid myocardial injury and performance feedback during CPR requires algorithms to analyze ventricular fibrillation signals. This report reviews investigations on different parameters of ventricular fibrillation electrocardiographic signals, including amplitude, frequency, bispectral analysis, amplitude spectrum area, wavelets, nonlinear dynamics, N(alpha) histograms, and combinations of several of these parameters. To date, no satisfactory methods have been found that cope with CPR artifacts and show adequate predictive power of successful defibrillation. The usual limitations of the studies are the small number of subjects, which precludes separation into training and test data. Because many investigations are animal studies of untreated short ventricular fibrillation, the results may be different for prolonged ventricular fibrillation in humans. The universality of threshold values has to be examined, and promising new parameters have to be monitored over longer time periods and analyzed for the effects of chest compressions, ventilation, and concomitant vasopressor therapy.

Algorithms↗
PubMed1989

Coronary artery bypass grafting in patients with ventricular fibrillation.

The role of coronary artery revascularization in the management of survivors of cardiac arrest remains controversial. Patients with sustained monomorphic ventricular tachycardia rarely respond to revascularization, but the response of patients with ventricular fibrillation as their basic arrhythmia has not been characterized. Coronary artery bypass grafting was performed in 8 patients with a history of cardiac arrest known to be caused by ventricular fibrillation without preceding sustained monomorphic ventricular tachycardia. All patients had critical double-vessel or triple-vessel coronary artery disease, and 7 of 8 had wall motion abnormalities from a prior myocardial infarction. After successful operation, 5 patients had no spontaneous arrhythmias and no inducible arrhythmias at a postoperative electrophysiological study. Three patients, however, had spontaneous, recurrent episodes of ventricular fibrillation unassociated with recurrent ischemia. Clinical factors were not useful predictors of response. The effect of coronary artery revascularization in patients with ventricular fibrillation is unpredictable, and full postoperative electrophysiological evaluation is necessary to judge the success of the procedure.

Cardiac Pacing, Artificial↗
PubMed1988

Prognosis of patients with ventricular tachycardia and ventricular fibrillation: role of the underlying etiology.

The prognosis of 149 patients with ventricular tachycardia (n = 108) or ventricular fibrillation (n = 41) was analyzed to assess the importance of the underlying etiology of the arrhythmia. Seventy-three patients (Group I) had a previous myocardial infarction and documented late sustained monomorphic ventricular tachycardia. Thirty-five (Group II) also had a previous myocardial infarction but had late ventricular fibrillation. There were 41 patients (Group III) without coronary artery disease: 9 patients with right ventricular dysplasia, 26 with idiopathic sustained ventricular tachycardia and 6 with idiopathic ventricular fibrillation. The mean follow-up period for all patients was 22 to 57 months. The total mortality rate in Group I (16%) and Group II (34%) and the arrhythmic mortality rate in Group I (5%) and Group II (11%) were significantly higher than the rates in Group III. In the latter group the total mortality rate was 4% for those with idiopathic ventricular tachycardia and 11% for those with right ventricular dysplasia, and there were no deaths due to arrhythmia (p less than 0.05). Left ventricular ejection fraction was significantly lower and left ventricular end-diastolic pressure was significantly higher in Group I and Group II than in Group III. There were nonfatal recurrences of ventricular tachycardia in 33 to 56% of patients, and the number of these episodes did not differ significantly in those with and without coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1979

Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes.

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.

Adult↗
PubMed1994

Stroke volume with dynamic cardiomyoplasty during ventricular fibrillation in the acute dog.

The objective of this study was to determine the pumping capability of dynamic cardiomyoplasty during induced ventricular fibrillation. In this acute study of 6 dogs, the pumping capability of the unconditioned left latissimus dorsi (LD) muscle (141 to 292 gm), wrapped around both ventricles, was investigated during induced ventricular fibrillation. Left-ventricular and femoral artery pressure, the ECG and aortic root flow velocity were monitored. Prior to inducing ventricular fibrillation, the ability of the unconditioned LD muscle to augment stroke volume (SV), was quantified as the area under the aortic flow-velocity record. The ventricles were then fibrillated and, after 10 sec, rhythmic 250 msec trains (1/sec) of stimuli (40/sec) were delivered to the thoracodorsal nerve to contract the LD muscle tetanically. In no case could dynamic cardiomyoplasty produce the same SV as when the ventricles were beating normally. In one animal, the SV attained two percent of the normal SV by 5 contractions; in another, the SV reached one percent by 25 contractions. In the remaining animals, the SV varied around 20% of the prefibrillation SV. By 90 contractions, the stroke volume was 10% of the prefibrillation value. The progressive decrease in SV was likely a consequence of LD muscle ischemia and fatigue, since the latissimus dorsi muscle provided low blood flow during the period of fibrillation.

Animals↗
PubMed1987

Serum potassium, calcium and magnesium after resuscitation from ventricular fibrillation: a canine study.

Serum electrolytes were measured before and sequentially for 3 hours after resuscitation from ventricular fibrillation in a canine model that was designed to approximate the human cardiac arrest and resuscitation process. Twenty anesthetized dogs were resuscitated from ventricular fibrillation; 7 required epinephrine during resuscitation and 13 did not. To control for the effects of anesthesia, 10 dogs were anesthetized and instrumented, but ventricular fibrillation was not induced. Serum potassium decreased from 3.7 +/- 0.3 mmol/liter at baseline to 3.2 +/- 0.4 mmol/liter 45 minutes after resuscitation in the experimental dogs resuscitated without epinephrine, as compared with 3.6 +/- 0.3 to 3.4 +/- 0.2 mmol/liter in control dogs (p = 0.07 versus control dogs by two-way analysis of variance) and returned toward baseline at the end of 3 hours. Serum calcium decreased from 9.6 +/- 0.6 mg/dl at baseline to 8.9 +/- 0.9 mg/dl at 5 minutes after resuscitation as compared with 9.4 +/- 0.7 to 9.5 +/- 0.7 mg/dl in control dogs (p less than 0.05 versus control dogs) and returned to baseline by 3 hours. Serum magnesium decreased from 1.5 +/- 0.1 to 1.3 +/- 0.2 mEq/dl by 3 hours in resuscitated dogs as compared with 1.6 +/- 0.2 to 1.5 +/- 0.2 mEq/dl in control dogs (p = 0.06 versus control dogs). These changes in serum potassium, calcium and magnesium were independent of the administration of epinephrine during the resuscitation process. Changes in potassium were independent of arterial pH or bicarbonate therapy. Serum glucose increased after ventricular fibrillation but not in control dogs (p less than 0.0005 versus control). No changes in other electrolytes were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

An external automatic device to detect ventricular fibrillation.

An analysis of a micro-processor-based system to detect cardiac arrest rhythms was made in a series of 84 cardiac arrests in 78 patients. The ECG was sensed using 2 external ECG/defibrillator pads applied to the chest wall. In 5 arrests, the initial rhythm was continuous electrical pacing in addition to the cardiac arrest and these were not included in the analysis. Of the remaining 79 arrests there were 15 in which the initial rhythm was ventricular fibrillation and 14 were correctly detected by the system (sensitivity 93%). In the remaining 64 arrests the initial rhythm was not ventricular fibrillation and 62 were correctly identified (specificity 97%). A high specificity is required in any device employing automatic detection of ventricular fibrillation. Continuous electrocardiographic recordings of the cardiac arrests were analysed every 8 to 18 s: of 223 sections showing ventricular fibrillation, 165 were correctly determined by the system, i.e. sensitivity 74%, where the rhythm was not ventricular fibrillation, of the 5002 sections 4953 were correctly detected by the system, i.e. specificity 99%. The percentage accuracy of detection of ventricular fibrillation varied from 25-100% (mean 81%) and for detection of non-ventricular fibrillation from 57-100% (mean 99%) in every 8 to 18 s section of ECG tracing per cardiac arrest episode. Thus the automatic detection of cardiac arrest rhythms is feasible with a high degree of accuracy.

Adolescent↗
PubMed1987

Increased incidence of isoproterenol-induced ventricular fibrillation in aging rats.

Prolonged beta-adrenergic stimulation obtained by subcutaneous injection of isoproterenol in unanesthetized, unrestrained rats elicited ventricular fibrillation in approximately 80% of animals at 10-12 months of age. Ventricular fibrillation failed to occur in 1-month-old rats and involved only 12% of rats at 2 months. Senescence appeared not to increase the frequency of ventricular fibrillation since a similar incidence was seen in rats at 10-12 and 19-21 months. In all instances, ventricular fibrillation was preceded by ECG changes consistent with acute subendocardial ischemia. To evaluate whether acute beta-adrenergic stimulation elicits comparable cardiovascular effects in animals of different age, a dose-response curve to intravenous injection of isoproterenol was performed in anesthetized rats. Changes in heart rate, systemic arterial pressure, left ventricular pressure, and dP/dt were not different among animal groups. It was concluded that the arrhythmogenic potential of isoproterenol may not be related to differences in cardiac beta-receptor sensitivity with age as suggested by the comparable changes in the inotropic and chronotropic actions of isoproterenol in the animal groups studied.

Aging↗
PubMed1992

Analysis of determinants of ventricular fibrillation induced by reperfusion: dissociation between electrical instability and myocardial damage.

To assess the underlying mechanisms of ventricular fibrillation induced by myocardial reperfusion after cardioplegic arrest, 62 patients undergoing an open heart operation were divided into two groups based on the absence (group 1, n = 37) or the development (group 2, n = 25) of reperfusion-induced ventricular fibrillation. There was no close relationship between the incidence of reperfusion-induced ventricular fibrillation and aortic clamp time. On reperfusion, the time to onset of cardiac activity was similar in groups 1 (2.4 +/- 1.8 minutes) and 2 (1.9 +/- 1.1 minutes). At that time, there was no significant difference in values of arterial oxygen and bicarbonate contents, pH, or base excess between the two groups, but myocardial temperature was significantly higher in group 2 (25.6 degrees +/- 3.4 degrees versus 27.6 degrees +/- 2.4 degrees C; p less than 0.05). In addition, serum levels of sodium (123.9 +/- 4.2 versus 126.1 +/- 3.7 mmol/L; p less than 0.05) and calcium (0.80 +/- 0.07 versus 0.84 +/- 0.05 mmol/L; p less than 0.05) were significantly higher and serum potassium levels (3.98 +/- 0.58 versus 3.55 +/- 0.61 mmol/L; p less than 0.02) and the serum potassium to calcium ratio (4.94 +/- 0.90 versus 4.29 +/- 0.72; p less than 0.01) significantly lower in group 2. Postoperative serum levels of the myocardial-specific isoenzyme of creatine kinase and myoglobin were similar in both groups. By multivariate analysis, shorter ischemic time, higher myocardial temperature, higher serum sodium concentration, and lower serum potassium to calcium ratio were found to influence induction of reperfusion-induced ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Temperature↗
PubMed1985

A new model of ventricular fibrillation induced by isoprenaline and catechol-O-methyl transferase inhibitor at a high perfusion temperature in isolated rat hearts.

Isolated rat hearts were perfused with various concentrations of isoprenaline (0.01-10 mumol/liter) for 30 min at a constant flow rate (6.5 ml/min) at 37-44 degrees C. The occurrence of ventricular fibrillations was isoprenaline concentration dependent and also perfusion temperature dependent in the combined treatment with various concentrations of isoprenaline and high perfusion temperatures. When the hearts were perfused with isoprenaline (1 mumol/liter) in the presence of tropolone (100 mumol/liter) at 40-41 degrees C, the duration of ventricular fibrillations was significantly prolonged, but the incidence of ventricular fibrillations was similar to that produced with isoprenaline (1 mumol/liter) alone. The antiarrhythmic drugs such as quinidine sulfate, lidocaine hydrochloride, dl-propranolol hydrochloride, carteolol hydrochloride, atenolol, dl-verapamil hydrochloride, and diltiazem hydrochloride, given at a concentration of 10 mumol/liter, significantly suppressed the incidence and duration of such ventricular fibrillations. Bretylium tosylate (10 mumol/liter) significantly suppressed the duration of the ventricular fibrillations but not their incidence. These results indicate that ventricular fibrillation induced by combined treatment with a high concentration of isoprenaline and tropolone at a high perfusion temperature in isolated rat hearts is a more useful experimental model of arrhythmia than conventional models.

Animals↗