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PubMed2004

Cardiopulmonary resuscitation (CPR) using periodic acceleration (pGz) in an older porcine model of ventricular fibrillation.

Cardiopulmonary resuscitation (CPR) can be achieved by repetitive motion of the body headwards to footwards in the spinal axis, at 2 Hz and +/- 0.6 G in a juvenile pig model of ventricular fibrillation. Return of spontaneous circulation and normal neurological outcome occurred after a total of 22 min of ventricular fibrillation that included a 3-min noninterventional period [Resuscitation 56 (2003) 215; Resuscitation 51 (2001) 55]. Since older pigs have stiffer rib cages than juvenile pigs and their hemodynamic response to various stimuli might differ, this study was carried out to determine whether this method of CPR, termed pGz-CPR, was just as effective in older pigs. pGz-CPR was also compared to chest compression CPR using an automated mechanical device (CONV-CPR). Ventricular fibrillation was instituted in older pigs weighing 23-34 kg and a 3-min noninterventional period was observed, followed by 15 min pGz-CPR in eight pigs or 15 min CONV-CPR in eight pigs. Return of spontaneous circulation (ROSC) occurred after defibrillation in all eight pigs with pGz-CPR and in six of eight pigs with CONV-CPR. Two of eight pigs with CONV-CPR and none of the eight pigs with pGz-CPR had rib fractures. Hemodynamic instability 15 min after ROSC occurred in all animals with CONV-CPR whereas only three of eight pigs with pGz-CPR demonstrated hemodynamic instability (P < 0.05). We conclude that pGz-CPR in older pigs produces similar ROSC reported by other investigators in pigs without the risk of rib fractures. Further, pGz-CPR is associated with a lower incidence of periods of hemodynamic instability following ROSC than CONV-CPR.

Acceleration↗
PubMedDate not supplied

High-frequency periodic sources underlie ventricular fibrillation in the isolated rabbit heart.

The mechanism(s) underlying ventricular fibrillation (VF) remain unclear. We hypothesized that at least some forms of VF are not random and that high-frequency periodic sources of activity manifest themselves as spatiotemporal periodicities, which drive VF. Twenty-four VF episodes from 8 Langendorff-perfused rabbit hearts were studied using high-resolution video imaging in conjunction with ECG recordings and spectral analysis. Sequential wavefronts that activated the ventricles in a spatially and temporally periodic fashion were identified. In addition, we analyzed the lifespan and dynamics of wavelets in VF, using a new method of phase mapping that enables identification of phase singularity points (PSs), which flank individual wavelets. Spatiotemporal periodicity was found in 21 of 24 episodes. Complete reentry on the epicardial surface was observed in 3 of 24 episodes. The cycle length of discrete regions of spatiotemporal periodicity correlated highly with the dominant frequency of the optical pseudo-ECG (R(2)=0.75) and with the global bipolar electrogram (R(2)=0.79). The lifespan of PSs was short (14.7+/-14.4 ms); 98% of PSs existed for <1 rotation. The mean number of waves entering (6.50+/-0.69) exceeded the mean number of waves that exited our mapping field (4.25+/-0.56; P<0.05). These results strongly suggest that ongoing stable sources are responsible for the majority of the frequency content of VF and therefore play a role in its maintenance. In this model, multiple wavelets resulting from wavebreaks do not appear to be responsible for the sustenance of this arrhythmia, but are rather the consequence of breakup of high-frequency activation from a dominant reentrant source.

Animals↗
PubMed1982

Ventricular fibrillation complicating acute myocardial infarction: reasons against the routine use of lidocaine.

Because of recent recommendations that lidocaine be used prophylactically in all coronary care unit (CCU) patients with suspected myocardial infarction (MI), an approach not used in our CCU, we analysed our experience with ventricular fibrillation (VF) occurring in the setting of an acute MI. The frequency of VF in all patients was 3.2%. In MI patients 5.7%, of primary ventricular fibrillation (PVF) 2.8%, and of complicating ventricular fibrillation (CVF) 6.8%. All patients with PVF were resuscitated immediately. There was an increased in-hospital mortality for patients with VF compared to patients without VF; however, the increased mortality did not seem to result directly from VF. The long-term survival of PVF patients who survived to discharge was excellent (80% at 58 months). The routine use of prophylactic lidocaine would have been of no potential benefit in 96.8% of our patients, subjecting them to extra expense and possible toxicity. Since we have found no compelling evidence that the prophylactic administration of lidocaine can reduce mortality, we do not recommend this therapy for acute MI patients in our CCU.

Aged↗
PubMed1993

[Ventricular fibrillation during stress test on a treadmill. Apropos of a case].

A case of ventricular fibrillation occurring in the recovery phase of treadmill exercise test is described. A 64-year-old man was admitted to the hospital because of chest pain. The resting electrocardiogram was normal, but during a stress test (Bruce protocol) ventricular ectopic beats and ischemic S-T depression were observed. The echocardiogram showed septal hypertrophy and septal and apical hypokinesia. Ten days later he, during antianginal therapy, underwent treadmill exercise testing. In contrast with the previous stress test, ventricular ectopic beats decreased during the effort, but the S-T segment depressed, at the third step, with mild chest pain and hypotension. While angina and electrocardiogram improved, suddenly ventricular fibrillation developed. The patient was successfully resuscitated with electrical defibrillation, with a 350 joules shock. Echocardiogram was unchanged; serum enzymes were slightly modified (secondary to DC-shock). The ischemic changes observed at the electrocardiogram in the anterior wall within seven days returned in the normal range. Ten days later the patient underwent cardiac catheterization. At ventriculography the posterior and diaphragmatic wall was diskinetic, ejection fraction was 70%; a complete occlusion of the right coronary artery at the origin, a critical stenosis of left descending artery, with occlusion in the middle tract were found. Circumflex artery was occluded at the origin with omo-etero-coronary collateral channels. Twenty days later, he had a successful bypass surgery. Postsurgical echocardiogram revealed a moderate depression of ejection fraction (41%), inferior diskinesia, apical hypokinesia, mild mitral regurgitation. The patient was discharged with digitalis, nitrates, aspirin and amiodarone for prophylactic treatment of paroxystic atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1959

The relation between temperature and changes in ion concentration on ventricular fibrillation induced electrically.

Further observations have been made on ventricular fibrillation induced by electrical stimulation in the isolated rabbit heart, in extension of the finding that fibrillation was arrested by cooling from 37 degrees to 32 degrees . The observations now made suggest that at 37 degrees the isolated rabbit heart perfused with Locke solution is on the edge of anoxia, but that at 32 degrees the oxygen supply is adequate. At the lower temperature the proportion of hearts fibrillating at any given potassium concentration was reduced, so, although the proportion of hearts fibrillating rose as the potassium concentration fell, even when the latter was one-quarter of the normal the proportion was not higher than 67%. The relation of the concentration of calcium ions to the proportion of hearts fibrillating changed from biphasic at 37 degrees to almost rectilinear at 32 degrees , the proportion increasing as the concentration of calcium ions rose. It was confirmed that a reduction in sodium concentration also raises the proportion of hearts fibrillating.

Animals↗
PubMed1993

Tacrine inhibits ventricular fibrillation induced by ischaemia and reperfusion and widens QT interval in rat.

OBJECTIVE: Tacrine was used as a tool to examine whether block of inward rectifying potassium current (IK1) represents a mechanism for suppression of arrhythmias induced by ischaemia and reperfusion. METHODS: Isolated rat hearts (n = 10-12 per group) were subjected to 30 min left regional ischaemia followed by reperfusion with and without tacrine. Rat heart was used to permit delayed rectifier (IK) block to be disregarded in interpretation of results (rat ventricle is deficient in functional IK). RESULTS: The incidence of ischaemia-induced ventricular fibrillation was reduced from 70% to 42%, 17% (p < 0.05), and 0% (p < 0.05) in hearts perfused with 0, 0.1, 1.0, and 10.0 microM tacrine. Likewise, the incidence of reperfusion induced ventricular fibrillation was reduced from 100% to 90%, 75%, and 50% (p < 0.05), respectively. Indirect evidence of repolarisation delay by tacrine was provided by QT widening; for example, 15 min after the onset of ischaemia, QT (at 100% repolarisation) was increased from 194(SEM 6) to 231(17), 235(13) (p < 0.05), and 341(24) ms (p < 0.05) by increasing concentrations of drug. QT interval measured in individual hearts during ischaemia correlated inversely with arrhythmia score (r2 = 0.392; p < 0.001). Tacrine had no effect on RR interval, coronary flow, recovery of flow during reperfusion, or occluded zone size. Tacrine caused bradycardia (significant at the 1.0 and 10.0 microM concentrations). In additional hearts (n = 12 per group), reversal of 10.0 microM tacrine-induced sinus bradycardia by left atrial pacing (5 Hz) significantly reduced tacrine induced QT widening (p < 0.05), and increased the incidence of ventricular fibrillation from 0% to 42% (although significant antiarrhythmic and QT widening effects were still present); 10.0 microM tacrine failed to reduce the incidence of reperfusion induced ventricular fibrillation in paced hearts (92% incidence v 100% in controls). CONCLUSIONS: The novel antiarrhythmic effects of tacrine, a drug with established blocking action on IK, IK1, and slow inward current, appear to result from QT widening in the rat (dependent partly on IK1 blockade in the ventricles and partly on drug induced sinus bradycardia).

Animals↗
PubMed1998

Relation between ventricular fibrillation voltage and probability of defibrillation shocks. Analysis using Hilbert transforms.

We used Hilbert transforms to re-evaluate the previously reported correlation between defibrillation shock outcome and absolute ventricular fibrillation voltage (AVFV). Previously in the literature, single values of AVFV acquired just prior to shock delivery were used to show a correlation between AVFV and shock outcome. In subsequent studies, a modified analysis procedure was used to show a correlation between shock outcome and moving average of AVFV. The use of single values of AVFV makes the AVFV sensitive to the local phase of the electrocardiographic (ECG) waveform, whereas moving averages are weighted by previous values of the ECG. The envelope is independent of the phase of the ECG and is not weighted by previous values of ECG as is the moving average. We explored, therefore, whether the AVFV computed from the envelopes of the ECG showed a stronger correlation with shock outcome than single values and moving averages of the AVFV. We estimated envelopes using the Hilbert transform. Orthogonal ECGs (sagittal, X; transverse, Y; and longitudinal, Z) were recorded from 11 dogs during 10 seconds of electrically induced ventricular fibrillation followed by a defibrillation shock with 50% probability of success. We used transvenous (right ventricular apex to subcutaneous patch) leads to deliver defibrillation shocks. Results from 236 successful and 249 unsuccessful trials showed, in contrast with the previously reported correlation, that moving average of AVFV was not higher for successful trials. In the Z direction, unsuccessful trials had higher voltage than successful trials (P < .05). Comparison of envelope voltages between successful and unsuccessful trials did not show any consistent and statistically significant differences. Although there were some methodological differences between ours and the previously reported studies, they are unlikely to have caused the discrepant observations. Our results suggest, therefore, that the absolute voltage of ECG during ventricular fibrillation is not robustly correlated with shock outcome.

Animals↗
PubMedDate not supplied

Comparison between the ventricular fibrillation thresholds of spontaneously hypertensive and normotensive rats--investigation of antidysrhythmic drugs.

Induction of ventricular fibrillation by intraventricular electric pulses is achieved with weaker currents in spontaneously hypertensive rats (SHR) than in normotensive rats of the Wistar-Kyoto (WKY) or Sprague-Dawley (SD) strains. The ventricular fibrillation threshold (VFT) is stable with time in SHR but not in WKY. Investigation of antidysrhythmic agents in SHR showed that most substances with membrane-stabilizing properties increase the VFT. There was no correlation between the elevation of VFT and the decrease in heart rate induced by the substances studied. Determination of the VFT in SHR may be useful for the screening of compounds with membrane-stabilizing properties.

Animals↗
PubMed2005

Cariporide minimizes adverse myocardial effects of epinephrine during resuscitation from ventricular fibrillation.

OBJECTIVE: Epinephrine given during closed-chest resuscitation increases blood flow across the coronary and cerebral circuits. However, epinephrine worsens reperfusion arrhythmias and intensifies postresuscitation myocardial dysfunction. We investigated whether cariporide-a selective sodium-hydrogen exchanger isoform-1 inhibitor-could ameliorate such adverse effects without diminishing its vasopressor actions. DESIGN: Randomized animal study. SETTING: University-based animal laboratory. SUBJECTS: Twenty-four anesthetized male domestic pigs (29-43 kg). INTERVENTIONS: Ventricular fibrillation was electrically induced and left untreated for 8 mins. Pigs were randomized to receive after 2 mins of chest compression a 3 mg/kg bolus of cariporide (n = 8), a 0.02 mg/kg bolus of epinephrine (n = 8), or a combination of cariporide and epinephrine (n = 8). Additional doses of epinephrine were given if the coronary perfusion pressure decreased below 15 mm Hg. Successfully resuscitated pigs were observed for 72 hrs. MEASUREMENTS AND MAIN RESULTS: The averaged coronary perfusion pressure was higher in the epinephrine (34 +/- 11 mm Hg, p = .001) and cariporide/epinephrine (35 +/- 10 mm Hg, p < .001) groups compared with the cariporide group (15 +/- 6 mm Hg). All pigs in the epinephrine and cariporide/epinephrine groups but only six in the cariporide group were successfully resuscitated and survived 72 hrs. During the immediate postresuscitation period, four of eight pigs in the epinephrine group had episodes of recurrent ventricular fibrillation or pulseless ventricular tachycardia requiring additional electrical shocks (7.0 +/- 6.4) but none in the cariporide and cariporide/epinephrine groups (chi-square, p = .008). Myocardial dysfunction occurred early after return of spontaneous circulation but only in the epinephrine group. CONCLUSIONS: The combined administration of cariporide and epinephrine prompted adequate pressor effects during chest compression and facilitated reestablishment of cardiac activity without episodes of recurrent ventricular fibrillation or transient myocardial dysfunction as with epinephrine alone.

Adrenergic beta-Agonists↗
PubMed1989

Ventricular fibrillation is reduced in hypothyroid rats with enhanced myocardial alpha-adrenoceptor responsiveness.

1. The severity of ventricular arrhythmias induced by coronary artery occlusion and reperfusion has been examined in control rats and animals made hypothyroid by pretreatment with 6-propylthiouracil (PTU). The maximal driving frequency and sensitivity of isolated left atria and papillary muscles to isoprenaline and to phenylephrine in the presence of propranolol, were also examined in tissues from control and hypothyroid animals. 2. Pretreatment with PTU resulted in a potentiation of responses to the alpha-adrenoceptor agonist phenylephrine in both left atria and papillary muscles, while responses to isoprenaline were depressed in left atria but unaltered in papillary muscles from hypothyroid animals. 3. In rats subject to coronary artery occlusion, PTU pretreatment reduced the incidence of ventricular fibrillation during acute myocardial ischaemia and abolished reperfusion-induced ventricular fibrillation. Mortality during myocardial ischaemia and reperfusion was also abolished. Diastolic blood pressure was similar in hypothyroid and control animals, but there was a small reduction in systolic blood pressure and a marked decrease in heart rate in PTU pretreated animals. 4. These results demonstrate that PTU-induced hypothyroidism represents a condition where cardiac alpha-adrenoceptor-mediated responses are enhanced but the severity of ischaemia- and reperfusion-induced arrhythmias is reduced.

Anesthesia↗
PubMedDate not supplied

Ventricular fibrillation during acute rejection after heart transplantation.

The case of a 46-year-old patient who underwent orthotopic heart transplantation for treatment of end-stage heart failure as a result of ischemic heart disease is reported. Four months after transplantation a grade II rejection episode was complicated by ventricular fibrillation. Lidocaine and procainamide intravenously did not effectively prevent recurrence. An increase of antirejection therapy in combination with flecainide acetate effectively prevented further episodes of ventricular fibrillation. This case demonstrates that recurrent ventricular fibrillation can be a complication of acute rejection.

Electrocardiography↗
PubMed1983

Verapamil for refractory ventricular fibrillation during cardiac operations in patients with cardiac hypertrophy.

Calcium-entry blockers prevent ventricular fibrillation during acute myocardial ischemia in laboratory animals. They may be useful as an adjunct to cold cardioplegia by preserving the myocardium during cardiopulmonary bypass. Their use may limit myocardial infarct size. However, the clinical application of calcium-entry blockers for ventricular dysrhythmias associated with myocardial ischemia has been little explored, as yet. We describe four patients, all of whom had significant cardiac hypertrophy (two had idiopathic hypertrophic subaortic stenosis; one had transposition of great vessels; and one had aortic stenosis) and in whom ventricular fibrillation developed after rewarming or shortly after the termination of bypass. The dysrhythmias were refractory to multiple attempts at defibrillation and conventional pharmacologic interventions. However, in each case, defibrillation was successful after administration of verapamil.

Adolescent↗
PubMed1981

The transition to ventricular fibrillation induced by reperfusion after acute ischemia in the dog: a period of organized epicardial activation.

Ventricular fibrillation was induced in eight of 10 open-chest dogs by reperfusion after a 15-minute occlusion of the proximal circumflex coronary artery. Simultaneous recordings were made from 27 epicardial electrodes spaced over both ventricles. Analysis of the initial 1.5--2.5 seconds of the transition from sinus rhythm or ventricular tachycardia to fibrillation revealed that ventricular activation occurred in an orderly, rapidly repeating sequence in all hearts. Each activation from arose near the border of the ischemic-reperfused region and passed across the nonischemic portion of the ventricles to the opposite side of the heart as a single, organized wavefront. As the arrhythmia progressed, the time between the appearance of successive activation fronts on the epicardium decreased. Concurrently, the time for each activation front to traverse the ventricles increased. The stimulation increase in rate of appearance and decrease in conduction velocity for each successive cycle resulted in overlapping cycles in which a new activation front arose from the ischemic-reperfused region before the previous front terminated over the right ventricle. The overlap between successive activation fronts increased as the arrhythmia continued. Thus, ventricular activation during the transition to ventricular fibrillation arose near the border of the ischemic-reperfused region and was organized as it passed across the nonischemic tissue, but the body surface ECG appeared disorganized because of variable spacing between successive, coexistent activation fronts.

Acute Disease↗
PubMed1994

Integration of absolute ventricular fibrillation voltage correlates with successful defibrillation.

Previous work has suggested that at higher absolute ventricular fibrillation voltages (AVFV), the heart is more amenable to defibrillation. This study investigated in a canine model whether voltage integration of the AVFV is associated with the defibrillation success rate. The moving-average filter was used to process the ventricular fibrillation (VF) waveform recorded from Lead II of the electrocardiogram (ECG). In seven animals, defibrillation trials were analyzed using a dc shock (DCS) successful approximately 50% of the time when delivered randomly. For each of a total of 84 DCS (40% successes, 60% failures), the fibrillation waveform just prior to DCS was analyzed. The integration of the AVFV waveform was performed over various sample sizes including 1, 4, 8, 16, 64, and 128 ms, as well as the time equal to the mean VF cycle length. The results suggest that dc shocks delivered at instants of higher values of integrated AVFV over the various window sizes are associated with successful defibrillation. Window sizes less than 16 ms appeared to offer the best discrimination. The integration of AVFV over the entire VF cycle length was significantly higher for successful rather than unsuccessful DCS. This interesting observation is consistent with the clinical observation that "coarse" VF (high AVFV) is easier to defibrillate than "fine" VF (low AVFV). The use of voltage integration of AVFV may have potential implications in the improvement of defibrillation success in implantable devices.

Analysis of Variance↗
PubMed1975

Ventricular fibrillation. Its effect on myocardial flow, distribution, and performance.

Subendocardial ischemia develops in hearts that are fibrillated during cardiopulmonary bypass when: (1) the normal ventricle is fibrillated with a sustained electrical stimulus, (2) the hypertrophied ventricle is allowed to fibrillate spontaneously, (3) the fibrillating heart becomes distended, or (4) the perfusion pressure is reduced to approximately 50 mm Hg. Myocardial hypothermia reduces cardiac oxygen requirements during fibrillation but does not prevent ischemia when perfusion pressure falls to levels frequently attained during clinical open-heart operations. The ischemia occurs because flow cannot rise sufficiently to meet the metabolic demands of ventricular fibrillation. The forces interacting to impede adequate flow to the subendocardium during ventricular fibrillation are: (1) the compressive forces exerted on subendocardial muscle by the strength of fibrillation, (2) the compressive forces resulting from raised intracavitary pressure due to occlusion or malfunction of the ventricular vent, and (3) the evolution of myocardial edema as ischemia is prolonged. We have abandoned the use of ventricular fibrillation in clinical open-heart operations and now allow the heart to beat continually with adequate perfusion pressure. We have not needed to use inotropic drugs postoperatively after aortic or mitral valve replacement since adopting this technique.

Aortic Valve↗
PubMed2004

Decrease in the occurrence of ventricular fibrillation as the initially observed arrhythmia after out-of-hospital cardiac arrest during 11 years in Sweden.

AIM: To describe the change in the occurrence of ventricular fibrillation as initially observed arrhythmia among patients suffering from out-of-hospital cardiac arrest in Sweden. PATIENTS: All patients included in the Swedish cardiac arrest registry between 1991 until 2001. The registry covers 85% of the population in Sweden. METHODS: All patients with bystander witnessed out-of-hospital cardiac arrest included in the Swedish Cardiac Arrest Registry between 1991 and 2001 from the same ambulance organisation each year were included in the survey. RESULTS: Over 11 years, among patients in Sweden with a bystander witnessed out-of-hospital cardiac arrest in whom cardiopulmonary resuscitation (CPR) was attempted (n = 9666), the occurrence of ventricular fibrillation as the initially obseved arrhythmia decreased from 45% in 1991 to 28% in 2001 (P < 0.0001) if the arrest occurred at home, and from 57% to 41% if the arrest occurred outside home (P < 0.0001). This was found despite the fact that the proportion who received bystander CPR increased from 29% in 1991 to 39% in 2001 if the arrest occurred at home (P < 0.0001) and from 54% to 60% if the arrest occurred outside home (NS). There was a significant increase in age among patients with out-of-hospital cardiac arrest at home, no change in the estimated interval between collapse and call but an increase in the interval between call and arrival of the ambulance among patients with out-of-hospital cardiac arrest outside home. CONCLUSION: During 11 years in Sweden, there was a marked decrease in the proportion of patients found in ventricular fibrillation among patients with a bystander witnessed cardiac arrest regardless whether the arrest occurred at home or outside home. A modest increase in age and interval between call for, and arrival of, the ambulance was associated with these findings.

Age Factors↗
PubMed1988

Ventricular fibrillation induced by the interaction between acute myocardial ischemia and sympathetic hyperactivity: effect of nifedipine.

Sympathetic hyperactivity plays a major role in the genesis of malignant arrhythmias during acute myocardial ischemia. An experimental model in which life-threatening arrhythmias are specifically and consistently induced by the interaction between acute myocardial ischemia and left stellate ganglion stimulation has been developed in alpha-chloralose anesthetized cats. In this preparation, drugs that share antiischemic, antiadrenergic, and specific electrophysiologic effects, such as verapamil, diltiazem, and amiodarone, were most effective. To evaluate the relative role of these different properties in mediating the effect of antiarrhythmic drugs, we used this same model to test nifedipine, a calcium channel blocker that is able to counteract the consequences of sympathetic stimulation on coronary circulation but has no electrophysiologic properties at concentrations relevant in the clinical setting. Nifedipine (15 micrograms/kg) prevented the occurrence of ventricular fibrillation in 10 of 13 animals (77%). Its efficacy was independent of changes in the peripheral hemodynamics. Plasma concentrations of nifedipine were within the therapeutic range in humans. To evaluate if this rather striking protective effect was specifically related to the prevention of the deleterious consequences of sympathetic stimulation, the effect of nifedipine on ventricular fibrillation threshold was studied in an additional group of 13 cats in the nonischemic state, during acute myocardial ischemia and during ischemia plus sympathetic stimulation. Nifedipine did not modify ventricular fibrillation threshold in nonischemic or in ischemic conditions. However, nifedipine specifically prevented the further reduction in ventricular fibrillation threshold occurring when sympathetic stimulation was superimposed on acute ischemia. These data suggest that the extension of ischemic damage by sympathetic stimulation is an important progenitor of arrhythmogenic action during acute ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗