SEARCH · PubMed Health

Results for “VENTRICULAR FIBRILLATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources

PubMed1998

Accurate recognition and effective treatment of ventricular fibrillation by automated external defibrillators in adolescents.

OBJECTIVES: To evaluate the accuracy and efficacy of automated external defibrillators (AEDs) in patients <16 years old. BACKGROUND: AEDs are standard therapy in out-of-hospital resuscitation of adults and have led to higher success rates. Their use in children and adolescents has never been evaluated, despite recommendations from the American Heart Association that they be used in children >8 years of age. METHODS: This was a retrospective cohort study of children <16 years old who underwent out-of-hospital cardiac resuscitation and on whom an AED was used during the resuscitation. The setting was rural and urban prehospital emergency medical systems. Patients were identified by review of a database of cardiac arrests maintained by a large surveillance program of these services. RESULTS: AEDs were used to assess cardiac rhythm in 18 patients with a mean age of 12.1 +/- 3.7 years. The cardiac rhythms were analyzed 67 times and included ventricular fibrillation (25), asystole/pulseless electrical activity (32), sinus bradycardia (6), and sinus tachycardia (4). The AEDs recognized all nonshockable rhythms accurately and advised no shock. Ventricular fibrillation was recognized accurately in 22 (88%) of 25 episodes and advised or administered a shock 22 times. Sensitivity and specificity for accurate rhythm analysis were 88% and 100%, respectively. One patient with a nonshockable rhythm survived, whereas 3 of 9 patients with ventricular fibrillation survived. CONCLUSIONS: These data furnish evidence that AEDs provide accurate rhythm detection and shock delivery to children and young adolescents. AED use is potentially as effective for children as it is for adults.

Adolescent↗

PubMed1992

Myocardial energetics during ventricular fibrillation investigated by magnetization transfer nuclear magnetic resonance spectroscopy.

Ventricular fibrillation (VF) is known to produce alterations in myocardial energetics, but the mechanism of these changes remains unclear. To investigate energy metabolism during VF, phosphorus nuclear magnetic resonance spectroscopy and magnetization transfer were applied to isolated perfused ferret hearts. VF was induced either by perfusion with digitalis (strophanthidin, 30 microM) or by high-frequency electrical stimulation. We measured the flux in two critical reactions: from inorganic phosphate (Pi) to ATP (ATP synthesis rate) and from phosphocreatine (PCr) to ATP (energy transfer capacity). During digitalis-induced VF, energy-related phosphates showed changes similar to those during hypoxia: myocardial [Pi] increased and [PCr] decreased. Concomitantly, the ATP synthesis rate increased to levels about threefold higher than control, whereas oxygen consumption increased by only 16%. The ATP synthesis rate exhibited a strong negative correlation with left ventricular pressure during VF (r = -0.95, n = 5, p < 0.02), whereas oxygen consumption did not (r = 0.19, p > 0.05). On the other hand, energy transfer capacity catalyzed by creatine kinase was significantly smaller during VF than in the control condition but still higher than the simultaneous ATP synthesis rate. In contrast to the marked energetic deterioration during VF induced by digitalis, electrically induced VF led to only a small increase in [Pi] and a small decrease in [PCr], and there were no significant changes in the ATP synthesis rate, energy transfer capacity, or O2 consumption. These results indicate that the rundown in energy metabolism during VF induced by digitalis was mainly attributable to a limitation of energy production through oxidative phosphorylation as well as to a marked increase in energy consumption. In contrast, myocardial energy generation remained unimpaired during VF induced by electrical stimulation. Intracellular calcium overload is more severe during VF induced by digitalis than during electrically induced VF (Circ Res 1991;68:1378-1389); severe calcium overload would be expected to compromise the capacity for energy generation by mitochondria. Thus, we propose that known differences in cellular calcium loading underlie the discrepant energetic patterns of the two types of VF.

Animals↗

PubMed1982

The effects of diltiazem and reduced serum ionized calcium on ischemic ventricular fibrillation in the dog.

Calcium influx blockers reportedly suppress ventricular arrhythmias during acute ischemia. We therefore studied the effects of diltiazem and reduced serum ionized calcium on ventricular fibrillation (VF) in a reversible ligation model. VF was produced at 15-minute intervals by simultaneous occlusion of the left anterior descending and circumflex arteries of 31 dogs. Time from coronary occlusion to onset of VF showed no significant variation during 15 consecutive trials in six dogs that received saline alone. Intravenous infusion of diltiazem (0.02 mg/kg per min) markedly delayed the onset of VF in each of 10 dogs (P less than 0.0001). Mean VF latency increased from 138 to 295 seconds during a 45-minute diltiazem infusion, declined exponentially when the infusion ceased, and was strongly correlated with serum diltiazem concentration (r = 0.96, P less than 10(-6)). In five dogs, hemodynamic measurements, including coronary venous blood flow, were performed during each occlusion. The increase in VF latency by diltiazem was not due to increased coronary flow during occlusion or to reduction of left ventricular (LV) mechanical work. In six dogs, mean serum ionized calcium, [Ca++], was reduced from 1.11 to 0.59 mM by infusion of sodium citrate. Citrate infusion increased mean VF latency from 155 to 243 seconds, and the increase observed in each dog was correlated (r = 0.84, P less than 10(-6)) with the reduction in [Ca++]. VF latency was unaffected by lidocaine in nine dogs. The antifibrillatory effect of diltiazem during global LV ischemia may be an electrophysiological phenomenon related to reduction of cellular calcium influx.

Animals↗

PubMed1993

[Ventricular fibrillation in a patient with mitral valve prolapse syndrome].

A patient with mitral valve prolapse who had cardiac arrest as a result of ventricular fibrillation is described. After two weeks of unconsciousness all brain functions gradually improved and full intellectual efficiency was regained. Exact study of the case did not reveal any other possible reason for ventricular fibrillation but mitral valve prolapse syndrome.

Adult↗

PubMed1994

Reperfusion ventricular fibrillation and electric countershocks during coronary artery bypass operations--association with postoperative CK-MB release.

Reperfusion ventricular fibrillation during coronary artery bypass surgery is common and electric shocks are often needed to terminate it. Both the fibrillation and the reversing electric shocks are potentially detrimental to the myocardium. In 61 aortocoronary bypass patients with uncomplicated clinical course (no difficulties in weaning from bypass, no ECG changes and no inotropic medication), serial creatine kinase-MB values were recorded. Evaluated explanatory variables were patient age, ejection fraction, aortic occlusion time, perfusion time, number of peripheral anastomoses and of anastomoses to marginal branches, myocardial fibrillation time before aortic cross-clamping, after cross-clamping prior to cardiac arrest and after declamping, and number of defibrillations. The results indicated that reperfusion fibrillation times up to 10 minutes are not harmful, provided that left ventricular decompression is carried out. Too early and thus numerous defibrillations raise creatine kinase-MB levels and probably also damage the myocardium, and therefore should be avoided.

Adult↗

PubMed2004

Prevention of primary ventricular fibrillation in acute myocardial infarction with prophylactic lidocaine.

Primary ventricular fibrillation (VF) during an acute myocardial infarction (AMI) occurs with a high incidence and mortality rate with or without thrombolysis. The incidence varies from 2% to 19% depending on the definition of "primary." Primary VF in this study refers to fibrillation occurring in the absence of shock or pulmonary edema. Mortality rate, when primary VF occurs, is 2 to 4 times greater than when it does not. Prevention of VF has been impeded by the publication of the 1996 recommendations of the American Heart Association and American College of Cardiology against the use of prophylactic lidocaine based on meta-analysis studies implying toxicity. This observational study of 4,254 patients with AMI reports the incidence and mortality rates of primary VF over 32 years. Of the 4,254 patients, 4,150 received prophylactic lidocaine, and 104 patients did not receive prophylactic lidocaine due to the 1996 guidelines, after which administration of prophylactic lidocaine was governed by physician choice. The incidence of primary VF was 0.5% among the 4,150 who received prophylactic lidocaine and 10% among the 104 who did not (p <0.0001). Among the 4,150 receiving prophylactic lidocaine, sinoatrial block occurred in 0.5% and complete infranodal atrial ventricular block occurred in 0.2%, all secondary to the site of infarction (concurrent serum lidocaine levels were < 4 microg/ml). Asystole was an agonal rhythm in 4%; these patients had been off lidocaine for 48 hours. Mortality rates were 10.5% in patients without primary VF and 25% in patients with VF (p <0.001). Thus, prophylactic lidocaine markedly decreased the incidence of VF in 4,150 patients with AMI to 0.5% compared with trials before and after thrombolysis (2% to 19%) and with the 104 patients in this study who did not receive prophylactic lidocaine (10%). No lidocaine-induced sinoatrial or atrial ventricular block or asystole occurred.

Aged↗

PubMed1998

Idiopathic ventricular fibrillation: clinical, electrophysiologic characteristics and long-term outcomes.

The long-term prognosis, including risks of arrhythmic recurrence of idiopathic ventricular fibrillation (VF), is uncertain; moreover, the role of electrophysiologic study in the diagnosis and guiding of antiarrhythmic drugs therapy for idiopathic VF remains controversial. The purpose of this study was to study the clinical features, electrophysiologic characteristics and long-term clinical outcomes of six consecutive patients (five males) who had at least one episode of aborted cardiac arrest (5 patients) or syncope (1 patients) with documentation of ventricular fibrillation (VF) in the absence of apparent heart disease. Idiopathic VF was diagnosed by exclusion. All patients underwent the electrophysiologic study including intravenous antiarrhythmic drug testing. Recurrences of VF after therapy and the long-term outcomes were assessed. The mean age at the first episode was 43+/-19 years (range from 16 to 63 years). All patients had sustained VF induced by double (3 patients) or triple (3 patients) ventricular extrastimuli at a paced cycle length of 400 or 500 ms from the right ventricular apex. Intravenous procainamide and/or mexiletine could suppress the reinduction of sustained VF in 4 (67%) of 6 patients. Recurrence of VF (documented VF attack, sudden cardiac arrest or syncope) was observed in 3 (100%) of 3 patients who received procainamide or mexiletine alone. Four patients (including 3 patients who experienced recurrence) received amiodarone alone or in combination with mexiletine, and these drugs could effectively prevent recurrence of VF. One patient with exercise-induced VF remained asymptomatic without any treatment during a follow-up period of 95 months. Another patient received an implantable cardioverter-defibrillator without concomitant antiarrhythmic drug therapy and had no discharge of electrical shock during 28 months of follow-up. During a mean follow-up period of 64+/-40 months (range from 28 to 128 months), all the patients were alive except patient No. 2 who died of acute hepatic failure. In conclusion, electrophysiologic study is a reliable diagnostic method, but it was of limited value in guiding antiarrhythmic drug therapy for preventing recurrence of idiopathic VF. Class I drug alone was associated with a high recurrence rate (100%) despite predictions that it would be effective by the electrophysiologic study. Amiodarone alone or in combination with mexiletine effectively prevented the recurrence of VF during the long-term follow-up along with a favourable outcome.

Administration, Oral↗

PubMed1989

Successful biventricular circulatory support as a bridge to cardiac transplantation during prolonged ventricular fibrillation and asystole.

The indications for biventricular versus left ventricular mechanical circulatory support as a bridge to cardiac transplantation are not well established. In this study, 27 potential heart transplant candidates who were in imminent risk of dying before donor heart procurement were implanted with Thoratec prosthetic ventricles (21 biventricular and six left ventricular) at three medical centers. A total of 21 patients (16 biventricular and five left ventricular) underwent successful cardiac transplantation after 1-65 days of circulatory support, and 19 were discharged from the hospital. Seven of the patients (all biventricular; diagnoses: four cardiomyopathy, two acute myocardial infarction, one end-stage coronary artery disease plus acute myocardial infarction) had prolonged arrhythmias that normally would have been lethal (six cases of ventricular fibrillation from 2 to 22 days, one asystole for 3 hours), but complete support of the systemic and pulmonary circulations was maintained in all seven patients with biventricular devices. Mean systemic blood flow during this period (4.6 +/- 0.6 l/min) was unchanged compared with that during sinus rhythm. Six of these patients survived to receive heart transplants. The use of right plus left prosthetic ventricles does not prevent the occurrence of arrhythmias but removes the threat and simplifies patient management. We conclude that biventricular support is indicated in bridge-to-transplant patients with potentially lethal arrhythmias.

Adult↗

PubMed1993

Intracellular calcium chelator, BAPTA-AM, prevents cocaine-induced ventricular fibrillation.

Cocaine is a potent cardiac stimulant that can provoke lethal cardiac events, including ventricular fibrillation (VF). The cocaine-induced accumulation of intracellular calcium could contribute significantly to the development of these lethal arrhythmias. To test this hypothesis, VF was induced in 12 mongrel dogs by the combination of cocaine (1.0 mg/kg) and a 2-min coronary occlusion during exercise. This test without cocaine failed to induce arrhythmias. Pretreatment with the intracellular calcium-specific chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM; 1.0 mg/kg iv) prevented VF in 8 of 12 animals (P < 0.001) and delayed the onset of lethal arrhythmias in 3 of the remaining animals. Cocaine induced significant increases in left ventricular (LV) systolic pressure (control 154.7 +/- 8.7, cocaine 167.4 +/- 8.4 mmHg), heart rate (control 195.9 +/- 6.1, cocaine 222.3 +/- 10.6 beats/min), and LV maximum rate of pressure development (dP/dtmax; control 5,251 +/- 317.6, cocaine 6,016 +/- 435.1 mmHg/s). BAPTA-AM attenuated the increase in LV dP/dtmax (BAPTA-AM 4,591 +/- 479.3 mmHg/s) and LV systolic pressure (BAPTA-AM 154.5 +/- 6.8 mmHg). Because vascular muscle relaxation could contribute to the cardioprotection, the cocaine and exercise plus ischemia test was repeated after nitroprusside. The nitroprusside prevented cocaine-induced increases in LV systolic pressure but failed to prevent VF. These data suggest that BAPTA-AM may prevent cocaine-induced VF independently of its vascular actions.

Animals↗

PubMed2003

Adaptive pacing during ventricular fibrillation.

While it has been shown that pacing during ventricular fibrillation (VF) can capture a portion of the epicardium, little is known about the characteristics of the area captured or about whether adaptively changing the pacing rate during VF will increase the area captured. In six open-chested pigs, pacing during VF was performed from the center of a plaque containing 504 electrodes 2 mm apart in a21 x 24 array on the anterior right ventricle. Simultaneous recordings from the 504 electrodes were used to construct activation maps from which the area of epicardium captured by pacing was determined. Four pacing algorithms were examined: (1) fixed rate pacing at 95% of the median VF activation rate, (2 and 3) adaptive pacing in which the pacing timing and/or rate is reset in real time if capture is not obtained, and (4) pacing at a slowly increasing rate after initial capture. Regional capture, defined as control of the myocardium under at least 10 plaque electrodes, was achieved in 71% (92/129) of pacing episodes. The incidence of capture was not significantly different for pacing algorithms 1-3. The maximum area captured for each pacing episode with algorithms 1-3 was 3.8 +/- 2.0 cm2(mean +/- SD). Within each animal, the pattern of capture was similar among all pacing episodes, no matter which algorithm was use dr = 0.85 +/- 0.25). The region of greatest capture extended away from the pacing site along the long axis of the myocardial fibers. However, the area of captured epicardium toward the right ventricular side of the pacing electrode was 9.7 times greater than toward the left ventricular side. This principal direction toward the right ventricular side of the pacing electrode was the same direction traveled by the majority of VF activation fronts before capture occurred. The absence of recorded activations at the pacing site for 20 consecutive stimuli predicted 83% of the time that regional capture was present. With algorithm 4, the pacing rate could be increased 7.1%+/- 4.3%while maintaining capture; however, the area of capture progressively decreased as the pacing rate increased. While pacing from the anterior right ventricular epicardium during VF, the area of capture is repeatable and is markedly asymmetrical with almost 10 times as much epicardium captured on the side of the pacing electrode closest to the acute margin of the right ventricle as on the opposite side. This marked asymmetry is associated both with myofiber orientation and with the direction of spread of activation and hence the direction of dispersion of refractoriness during VF just before pacing is initiated. It is possible to perform adaptive pacing algorithms in real time during VF; however, the two adaptive algorithms tested did not capture significantly more epicardium than a simple fixed-rate pacing algorithm. Although it is possible to maintain capture while increasing the pacing rate during VF, the area of capture decreases.

Algorithms↗

PubMed1975

The effect of sympathomimetic amines on the ventricular fibrillation threshold in the rabbit isolated heart.

1 The ventricular fibrillation threshold (VFT) was measured in the isolated heart of the rabbit perfused via the aorta with McEwen's solution at 37 degrees C by applying a single 10 ms pulse of current during the vulnerable period of late systole. The arrhythmia induced was either fibrillation or a rapid tachycardia. 2 The catecholamines adrenaline, noradrenaline and isoprenaline, but not dopamine, when infused at rates which produced similar moderate effects on cardiac rate and force, significantly lowered the VFT; it was reduced slightly more by adrenaline than by the other two. Phenylephrine and methoxamine were ineffective. Only those sympathomimetic amines which lowered the VFT also shortened the vulnerable time, i.e. minimal time after the R-wave of the ECG at which the pulse had to be applied to induce the arrhythmia. 3 The lowering effect of adrenaline on the VFT was not influenced by phentolamine but was blocked by propranolol and pindolol. 4 Chloroform potentiated the lowering effect of adrenaline, but not that of isoprenaline, on the VFT. Carbachol did not alter the effect of adrenaline on the VFT. 5 The results indicate that adrenaline, noradrenaline and isoprenaline lower the VFT by a direct action on the cardiac musculature and that this effect is mediated via beta-adrenoceptors.

Amines↗

PubMed2004

Combined phase singularity and wavefront analysis for optical maps of ventricular fibrillation.

Much of the research into the mechanisms of ventricular fibrillation (VF) employs high-resolution mapping of electrical activation and recovery patterns. We previously developed a method for analyzing electrically mapped VF patterns that was based on identifying individual VF wavefronts. We now introduce a related method designed to take into account the information on repolarization that is present in optically mapped VF data. The new method first converts raw fluorescence data to an angular variable that tracks the phase of the mapped tissue through the depolarization-repolarization cycle. We define wavefronts in this context as isolines of phase that terminate either at boundaries or at singular points within the phase field. These singularities are the pivots of functional reentry and are important determinants of VF patterns. We parameterize VF by constructing data structures that describe wavefronts and singularities and also maintain wavefront-wavefront, wavefront-singularity, and singularity-singularity relationships. We describe one important application of this parameterization, which is to identify, localize, and characterize the importance of occurrences of propagation block during VF.

Action Potentials↗

PubMed1999

Linear and non-linear analysis of the surface electrocardiogram during human ventricular fibrillation shows evidence of order in the underlying mechanism.

Ventricular fibrillation (VF) is a poorly understood yet potentially lethal cardiac arrhythmia. The electrocardiogram (ECG) time series of VF is investigated by comparison of the linear and non-linear features of VF time series and surrogates in which internal correlations have been destroyed. From 40 ECG time series of human VF and 40 surrogate time series, three quantities are evaluated: the percentage of the linear time-frequency distribution (TFD) exceeding a threshold, the non-linear coarse-grained correlation dimension (Dcg), and the percentage of diagonal lines in the non-linear recurrence plot longer than 10 elements (D10). It is found that the mean (SD) percent threshold TFD and Dcg are higher for the surrogates (6.7% (1.3) and 5.3 (0.6)) than the VF time series (5.6% (0.7) and 3.8 (0.9)), whereas the mean D10 is higher for the VF time series (49% (13)) than the surrogates (32% (7)). All of these differences are significant (p < 0.0001) and indicate greater order in the VF time series than in the surrogates. It is therefore shown that both linear and non-linear signal analysis demonstrate order in the ECG time series of VF.

Electrocardiography↗

PubMed1981

Dependence of ventricular fibrillation propensity on coronary blood flow without myocardial ischemia.

Ventricular fibrillation threshold (VFT) changes have been linked to coronary blood flow (CBF) in the context of CBF reduction and subsequent myocardial hypoxia. To clarify the effect of CBF on VFT in the absence of myocardial hypoxia, 18 open-chest pentobarbital-anesthetized dogs with uniformly controlled heart rate, cardiac output, and mean systemic arterial pressure (SAP) were studied as follows: CBF, coronary sinus O2 content (CcsO2), and thereby myocardial O2 consumption were continuously monitored. Baseline VFT determined by the single stimulus scanning technique was 33.0 +/- 3.9 mA. Initial values of CBF index (I) and VFT (n = 18) were positively correlated (VFTmA = 0.8 +/- 0.245 . CBFI ml/min . 100g-1LV; r = 0.60, p less than 0.01). Stepwise CBFI increments up to five times in excess of initial 131.5 +/- 9.7 ml/min . 100g-1LV were then induced by changing in random order. SAP (n = 10), left coronary perfusion pressure (n = 7), and arterial O2 content (n = 10) with VFT determined at each step; CcsO2 remained above 5.5 vol% while CBFI and VFT changes were positively correlated, and mean weighted slope of VFTmA = 16.6 +/- 0.103 . CBFI ml/min . 100 g-1Lv (r = 0.82, p less than 0.05). Systemic or coronary perfusion pressure and arterial or coronary sinus O2 content did not appear to affect VFT independently. It is concluded that even in the absence of myocardial hypoxia, CBF itself is a major determinant of VFT and thereby of innate arrhythmogenic propensity.

Animals↗

PubMed1975

The effect of anoxia on the ventricular fibrillation threshold in the rabbit isolated heart.

1. The ventricular fibrillation threshold (VFT) was measured in the isolated heart of the rabbit perfused via the aorta with McEwen's solution at 37 degrees C by applying a single 10 ms pulse of current during the vulnerable period of late systole. The arrhythmia induced was either fibrillation or a rapid tachycardia. 2. Gassing the McEwen's solution with 5% CO2 in N2 (anoxia) instead of with carbogen caused a negative inotropic and chronotropic effect and significantly lowered the VFT. Although anoxia releases noradrenaline from the heart the effect of anoxia on the VFT was not prevented by beta-adrenoceptor blockade with propranolol or pindolol or by previous treatment with reserpine. 3. Perfusion with adenosine (5 muM) which is released from the heart muscle by anoxia, or with dipyridamole (10 muM) which protects the adenosine from binding or destruction by the tissues, or with both combined failed to alter the VFT significantly. Furthermore neither adenosine nor dipyridamole significantly altered the effect of anoxia on the VFT. 4. Anoxia, adenosine and dipyridamole significantly increased the duration of the induced arrhythmia when compared with that of the controls. 5. Anoxia and adenosine significantly shortened the vulnerable time, i.e., the minimal time after the R-wave of the ECG at which the pulse had to be applied to induce the arrhythmia. 6. Perfusion with the McEwen's solution gassed with 5% CO2 in air (hypoxia) significantly lowered the VFT but the effect was not as great as with anoxia. Isoprenaline when infused lowered the VFT but this effect was not potentiated by hypoxia. 7. The results indicate that (a) anoxia lowers the VFT in the perfused isolated heart of the rabbit and that this effect is not due to adenosine or noradrenaline released by the anoxia and (b) hypoxia does not sensitize the heart to the arrhythmic effect of isoprenaline.

Adenosine↗

PubMed1998

Lidocaine increases the ventricular fibrillation threshold during bupivacaine-induced cardiotoxicity in pigs.

Ventricular fibrillation (VF) is a cause of death in bupivacaine-induced cardiovascular toxicity. We have examined the therapeutic effects of lidocaine on the threshold for bupivacaine-induced VF in in situ beating swine hearts. Twenty-four animals were allocated to one of three groups: 0.25% bupivacaine, 1% lidocaine or 0.25% bupivacaine with 1% lidocaine were infused into the left anterior descending coronary artery in increasing doses of 0, 1, 2, 4, 8 and 16 ml h-1 for 15 min, respectively. ECG and haemodynamic variables were monitored continuously during infusion. Regional myocardial function in the area supplied by the left anterior descending coronary artery was assessed using the sonomicrometry technique. VF did not occur in the lidocaine group. VF developed at higher infusion rates in animals given bupivacaine with lidocaine (in one animal at an infusion rate of 8 ml h-1 and in seven at 16 ml h-1) compared with animals given bupivacaine alone (in one at an infusion rate of 4 and in seven at 8 ml h-1). Although regional myocardial function decreased with increases in the infusion rate in each group, the depressant effects of the bupivacaine solution (medial inhibitory infusion rate of systolic shortening: IR50 = 2.43 (0.43) ml h-1) were significantly greater than those of the lidocaine solution (IR50 = 5.83 (0.87) ml h-1), but did not differ from those of the bupivacaine with lidocaine solution (IR50 = 3.54 (0.56) ml h-1). This study indicates that a combination of lidocaine and bupivacaine increased the threshold for bupivacaine-induced VF without further depressing myocardial contractility.

Anesthetics, Combined↗

PubMed2001

Dynamics of intramural and transmural reentry during ventricular fibrillation in isolated swine ventricles.

The intramural dynamics of ventricular fibrillation (VF) remain poorly understood. Recent investigations have suggested that stable intramural reentry may underlie the mechanisms of VF. We performed optical mapping studies of VF in isolated swine right ventricles (RVs) and left ventricles (LVs). Nine RV walls were cut obliquely in their distal edge exposing the transmural surface. Six LV wedge preparations were also studied. Results showed that intramural reentry was present. In RV, 28 of 44 VF episodes showed reentry; 15% of the activation pathways were reentrant. Except for 4 episodes, reentry was transmural, involving subendocardial structures as the papillary muscle (PM) or trabeculae. In LV, reentry was observed in 27 of 27 VF episodes; 23% of the activations were part of reentrant pathways (P<0.05 compared with RV). All LV reentrant pathways were truly intramural (confined to the wall) and were frequently located at the PM insertion. In both ventricles, reentry was spatially and temporally unstable. Histological studies showed abrupt changes in fiber orientation at sites of reentry and wave splitting. Connexin 40 immunostaining demonstrated intramyocardial Purkinje fibers at sites of reentry in the PM root and around endocardial trabeculae. Our results confirm that reentry is frequent-but unstable-in the myocardial wall during VF. In RV, reentry is mostly transmural and requires participation of subendocardial structures. The LV has a greater incidence of reentry and is intramural. Anisotropic anatomic structures played key roles in the generation of wave splitting and in the maintenance of reentry.

Animals↗

PubMed1997

Estimation of the ventricular fibrillation duration by autoregressive modeling.

An accurate estimation of ventricular fibrillation (VF) duration could be critical in selecting the most effective therapeutic intervention. We test the hypothesis that changes in frequency content of VF signals can be quantified by using autoregressive (AR) modeling, and the duration since the onset of VF can be estimated by using this method. VF signals were recorded for up to 300 s in five isolated rabbit hearts. Fourth-order AR parameters of successive segments were estimated, and frequencies of the first poles (the pole with lower frequency) were pooled together and a curve was fitted: F(t) = A exp (-alpha t) + B, where F(t) is the estimated frequency of the first pole at t'th time instant, alpha is the decay constant, B is the offset frequency, and A is the frequency at time zero minus the offset frequency. The utility of this curve in estimating the VF duration was tested in four new experiments, and the difference between the actual and the estimated VF duration (estimation error) was calculated. F(t), the frequency of the first pole, decreased from 12 to 6 Hz with duration of:VF, while the frequency of the other pole decreased from 25 to 20 Hz. Parameters of the fitted curve were calculated as A = 7.8, alpha = 0.0041 and B was selected as four. Testing on a new set of VF signals produced very little estimation error for the first 100 s of VF, although this error increased with VF duration. For these new signals, the mean value of the absolute estimation error was 26 s. Results of this study show that changes in the frequency content of electrocardiogram (ECG) during VF can be quantified by AR modeling and that the frequency changes associated with a pole of this model can be used to estimate the VF duration.

Algorithms↗