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PubMed2002

Multiple spatially distributed stimulators and timing programs for entrainment of activation during ventricular fibrillation.

Activation sequences during ventricular fibrillation (VF) display complex pattern and fast rate. Recent evidence suggests that even during VF an excitable gap may exist. Existence of excitable gap lead us to hypothesize that it should be possible to entrain activation patterns during VF by using spatially distributed and temporally phased pacing strength stimuli. We describe here the electronics hardware and software that were developed to test our hypothesis. Eight biphasic stimulators were designed and fabricated, each addressable via a TTL input and thus independently triggered. To minimize electrical interference from stimulus pulses the stimulators were optically isolated. A program written in C was used to deliver TTL inputs to time the sequence of stimulation. The parameters that could be varied were, pulse intensity, polarity, and duration, inter pulse interval and activation pattern cycle length. Restitution's of action potential duration, conduction velocity, and complex activation patterns make the timing of stimulators complex. To aid in optimal timing of these stimulators, we used a Luo-Rudy ionic model of cellular activation to simulate VF in a matrix of 400 x 400 cells. Entrainment of activation was verified using animated displays of activation sequences. Using results of simulation we verified the function of our stimulators experimentally using electrically induced VF in canines and by using electrograms recorded from 121-electrode patch. Our results show that the developed hardware and software can be used to deliver distributed stimuli in a flexible and effective pattern, which may aid in development of approaches for treatment of VF.

Animals↗

PubMed1999

Mechanism of procainamide-induced prevention of spontaneous wave break during ventricular fibrillation. Insight into the maintenance of fibrillation wave fronts.

BACKGROUND: Ventricular fibrillation (VF) is maintained by 2 mechanisms: first by reentry formation and second by spontaneous wave break or wave splitting. We hypothesized that spontaneous wave break results from a critical shortening of the action potential duration (APD) during VF and that its prevention by procainamide eliminates spontaneous wave break. METHODS AND RESULTS: The endocardial surfaces of 7 isolated, perfused swine right ventricles were mapped with a 3.2x3.8 cm plaque with 477 bipolar electrodes. Activation pattern during VF was visualized dynamically while simultaneously recording epicardial action potentials with a glass microelectrode. APD restitution curves were constructed during VF (dynamic) and during S(1)S(2) protocols. At baseline, VF was maintained by 5.3+/-1 wavelets. Procainamide (PA) at 10 microgram/mL decreased the number of wavelets to 3.5+/-1 (P<0.05). At baseline VF was maintained by spontaneous wave break and by new reentrant wave front formation. PA eliminated spontaneous wave break during VF while having no effect on reentry formation. PA increased the cycle length of the VF (148.5+/-41.2 ms vs 81+/-10 ms, P<0.01) and the core area of the reentry from 5.8 to 14.5 mm(2) (P<0.05). Dynamic APD restitution curve during VF showed that PA eliminated the initiation of activation with APDs shorter than 30 ms. The effects of PA on cellular properties and wave front dynamics were reversed during 60 minutes of drug-free perfusion. CONCLUSIONS: Critically short APDs during VF promote spontaneous wave break. Their elimination with PA, however, maintains VF by generating new reentrant wave front.

Action Potentials↗

PubMed1999

External exponential biphasic versus monophasic shock waveform: efficacy in ventricular fibrillation of longer duration.

Ventricular fibrillation (VF) duration may be a factor in determining the defibrillation energy for successful defibrillation. Exponential biphasic waveforms have been shown to defibrillate with less energy than do monophasic waveforms when used for external defibrillation. However, it is unknown whether this advantage persists with longer VF duration. We tested the hypothesis that exponential biphasic waveforms have lower defibrillation energy as compared to exponential monophasic waveforms even with longer VF duration up to 1 minute. In a swine model of external defibrillation (n = 12, 35 +/- 6 kg), we determined the stored energy at 50% defibrillation success (E50) after both 10 seconds and 1 minute of VF duration. A single exponential monophasic (M) and two exponential biphasic (B1 and B2) waveforms were tested with the following characteristics: M (60 microF, 70% tilt), B1 (60/60 microF, 70% tilt/3 ms pulse width), and B2 (60/20 microF, 70% tilt/3 ms pulse width) where the ratio of the phase 2 leading edge voltage to that of phase 1 was 0.5 for B1 and 1.0 for B2. E50 was measured by a Bayesian technique with a total often defibrillation shocks in each waveform and VF duration randomly. The E50 (J) for M, B1, and B2 were 131 +/- 41, 57 +/- 18,* and 60 +/- 26* with 10 seconds of VF duration, respectively, and 114 +/- 62, 77 +/- 45,* and 72 +/- 53* with 1 minute of VF duration, respectively (*P < 0.05 vs M). There was no significant difference in the E50 between 10 seconds and 1 minute of VF durations for each waveform. We conclude that (1) the E50 does not significantly increase with lengthening VF durations up to 1 minute regardless of the shock waveform, and (2) external exponential biphasic shocks are more effective than monophasic waveforms even with longer VF durations.

Analysis of Variance↗

PubMed1981

Ventricular fibrillation and its recurrence in early acute myocardial infarction.

At the initial arrest in 73 consecutive survivors of primary ventricular fibrillation who were seen within 1 h of myocardial infarction, 67% had much less than 2 episodes of ventricular fibrillation and 57% required much less than 2 shocks: only 7% required greater than 10 shocks to correct ventricular fibrillation. 12 (16%) of the 73 had recurrent ventricular fibrillation. The incidence of recurrent ventricular fibrillation, number of recurrences, and interval from the initial episode to recurrent ventricular fibrillation were similar whether the initial episode occurred within the first hour of the onset of symptoms or later. Age, sex, history of previous infarction, site of infarction, adequacy of initial resuscitation, place of arrest, time from onset of symptoms to initial arrest, and delay before initial attempted defibrillation were not significantly related to the recurrence of ventricular fibrillation. The incidence of recurrent ventricular fibrillation among patients seen within 1 h of the onset of symptoms was not greater than among comparable patients seen later.

Acute Disease↗

PubMed1994

Changes in the surface electrocardiogram during the onset of spontaneous ventricular fibrillation in man.

The aim of this study was to quantify electrocardiographic changes during the onset and early stages of ventricular fibrillation. Thirty recordings of ventricular fibrillation (mean duration 57 s, range 24-160 s) were obtained from 23 Coronary Care Unit patients. Each recording was investigated using frequency analysis on 1 s epochs of data. A significant rise in the mean dominant frequency of ventricular fibrillation from 3.9 Hz (SD 0.8 Hz) to 5.9 Hz (SD 1.0 Hz) was observed between 1 s and 30 s (P < 0.0001). At the same time, the width of the dominant peak decreased significantly (P < 0.001) and the height of higher frequency harmonics fell (P < 0.01). There was no significant change in peak height as ventricular fibrillation evolved. This study shows that the electrocardiogram retains periodic characteristics during the first 30 s of ventricular fibrillation and that these periodic characteristics become concentrated in a progressively narrower band of frequencies. These findings would suggest that during the early stages of ventricular fibrillation myocardial activation is both accelerating and coherent, rather than incoherent as has been traditionally believed.

Electric Countershock↗

PubMed1970

Long-term prognosis following ventricular fibrillation in acute ischaemic heart disease.

Of 160 patients who survived ventricular fibrillation complicating acute ischaemic heart disease, 80 had had a clinically mild coronary attack. Most of the long-term survivors had ventricular fibrillation within 24 hours of the onset of symptoms. The longterm prognosis of the survivors was similar to that of patients whose myocardial infarction was not complicated by ventricular fibrillation. Those patients who survived ventricular fibrillation which occurred within four hours of the onset of symptoms were younger, usually had had a mild coronary attack, and had the most favourable longterm prognosis. The number of episodes of ventricular fibrillation did not affect adversely the long-term prognosis. Of those who at the time of review were eligible to work, 86% were fit to work and 68% were actually at work.

Acute Disease↗

PubMed2002

Metabolic causes and prevention of ventricular fibrillation during acute coronary syndromes.

The mechanisms leading to ventricular fibrillation that occur during acute myocardial ischemia are ill understood. Whether primary ventricular fibrillation is due to a transient imbalance of electrolytes, an alteration of membrane permeability, electrical re-entry phenomena, or other factors, one overriding influence is the development of regional myocardial energy crises. Acute alteration in the balance of substrate supply may lead, during greatly reduced blood flow, to instability of myocardial electrical conduction with the development of re-entry circuits. An immediate response to the angor animi and initial symptoms of an acute coronary syndrome is a rapid and marked increase in catecholamine release, which leads to adipose tissue lipolysis with an acute increase in plasma free fatty acid concentrations, suppression of insulin activity, and a reduction in glucose uptake by the myocardium. The utilization of free fatty acids instead of glucose by the ischemic myocardium could precipitate regional oxygen or energy crises. Prevention therefore should focus on minimizing the catecholamine response and providing the myocardium with an optimum supply of energy substrates. Since catecholamines are inotropic, the aim should be to redress the imbalance of substrate availability by controlling adipose lipolysis with reduction of plasma free fatty acid concentrations, increasing the availability of glucose, or both. Other approaches include inhibition of acylcarnitine transport and manipulation of fatty acid intermediaries. To combat primary ventricular fibrillation, preventive treatment must be established within 6 to 10 hours of the onset of ischemia. There is already experimental and clinical evidence that antilipolytic drugs decrease the incidence of ventricular fibrillation, but their potential has not been explored extensively.

Animals↗

PubMed1994

Considerations for ventricular fibrillation detection by implantable cardioverter defibrillators.

Implantable cardioverter defibrillator detection of ventricular fibrillation is inherently a complicated process. Nevertheless, there is a clinical imperative that ventricular fibrillation be detected with 100% sensitivity. Incumbent with the need for such a high sensitivity is a trade-off that results in diminished ventricular fibrillation detection specificity, which in turn results in unnecessary delivery of high-energy shocks. In this review we look in generic terms at the different lead and detection systems available and the effect of these systems on both undersensing and oversensing of ventricular fibrillation. In addition, several clinical and programming issues that affect sensitivity and specificity of ventricular fibrillation detection are reviewed.

Algorithms↗

PubMed1975

Influence of sympathetic tone on ventricular fibrillation threshold during experimental coronary occlusion.

The effects of increased and decreased cardiac sympathetic tone and coronary occlusion on ventricular fibrillation were determined in 14 open chest dogs anesthetized with sodium pentobarbital. Heart rate was kept constant by pacing the right atrium at cycle lengths of 500 msec. Ventricular fibrillation threshold was measured by delivering 350 msec trains of constant current stimuli with a frequency of 100 hertz and 2 msec duration. The minimal current of the train that induced fibrillation was taken as the ventricular fibrillation threshold. In seven animals, the effects of stellate stimulation were studied. Ventricular fibrillation threshold was measured during control periods, after 2 minutes of cornoary occlusion, after 2 minutes of stellate stimulation and after 2 minutes of stellate stimulation and coronary occlusion. Coronary occlusion alone decreased ventricular fibrillation threshold an average of 35 percent of control valvues and stellate stimulation alone decreased the threshold an average of 42 percent of control values. The combination of both these interventions decreased ventricular fibrillation threshold an average of 63 percent of control values. The effects of stellate ablation were studied in seven animals. Ventricular fibrillation threshold was measured during control periods, and during coronary occlusion before and after stellate ganglionectomy. Stellectomy increased the threshold an average of 31 percent above control values. After stellectomy, coronary occlusion decreased ventricular fibrillation threshold by only 11 percent of control values, a value 26 percent higher than the threshold during coronary occlusion before stellectomy. These findings may have therapeutic implications for the management of arrhythmias in patients with acute myocardial infarction or some forms of central nervous system disease.

Animals↗

PubMed1991

[Prognosis in early and late ventricular fibrillation after acute myocardial infarction].

Of 413 patients with in-hospital ventricular fibrillation complicating acute myocardial infarction 281 had early (less than 48 hours post infarction) ventricular fibrillation and 132 had late ventricular fibrillation. In-hospital and longterm prognoses were not influenced by time of ventricular fibrillation, but advanced age and signs of reduced left ventricular function were found to be independent significant risk factors for short and longterm prognoses.

Adult↗

PubMed1979

Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion.

The effect of nitroglycerin on vulnerability to ventricular fibrillation was examined in 44 chloralose-anesthetized dogs. In 19 animals ventricular fibrillation threshold was measured before and during a 10 minute period of occlusion of the left anterior descending coronary artery followed by abrupt release of occlusion. Fibrillation threshold was determined using the single stimulus and train of stimuli methods. The influence of nitroglycerin on vulnerability was assessed with and without prevention of the drug's hypotensive effect by intravenous injection of phenylephrine. In the nonischemic myocardium, infusion of nitroglycerin alone or in combination with phenylephrine did not alter the ventricular fibrillation threshold. However, during both coronary occlusion and reperfusion, administration of nitroglycerin alone afforded partial protection against vulnerability to ventricular fibrillation. Nearly complete protection was imparted by combined administration of nitroglycerin and phenylephrine. The incidence of spontaneous ventricular fibrillation during reperfusion was significantly reduced by combined administration of nitroglycerin and phenylephrine. It is concluded that infusion of nitroglycerin decreases susceptibility to ventricular fibrillation during both acute myocardial ischemia and reperfusion and that this beneficial action is substantially enhanced when the drug's hypotensive effect is prevented.

Animals↗

PubMed2004

[Recovery from fatal ventricular fibrillation after immediate application of percutaneous cardiopulmonary support].

We present a patient who recovered from refractory ventricular fibrillation after immediate application of percutaneous cardiopulmonary support (PCPS). On the postoperative day (POD) 3 after the Y-grafting surgery for abdominal aortic aneurysm, circulation collapsed due to sudden onset of ventricular fibrillation. Because ventricular fibrillation had persisted in spite of medical treatment and defibrillation, we established PCPS and his circulation recovered. Although an emergent coronary angiography revealed no new lesions, we performed an emergent percutaneous catheter intervention to deny the possibility that ischemic changes had contributed to the arrhythmia. Soon after percutaneous transluminal coronary angioplasty, we successfully weaned him from PCPS, and extubated his trachea on the POD 5 without any neurological deficits. On the POD 8, ventricular fibrillation occurred again and defibrillation was effective at this time. We suspected cardiac ischemia, prolonged QT interval, and electrical remodeling due to hypertrophic heart as possible causes of refractory ventricular fibrillation. Therefore, we performed percutaneous transluminal coronary angioplasty, terminated famotidine administration, maintained normal electrolytes level, started administration of beta-blocker, and implanted an cardioverter defibrillator. On the POD 16, he was discharged from the ICU with no neurological deficits.

Adrenergic beta-Antagonists↗

PubMed1988

Influence of ventricular fibrillation duration on defibrillation energy in dogs using bidirectional pulse discharges.

The automatic implantable defibrillator device typically discharges 5-30 seconds after detection of ventricular fibrillation. To investigate the importance of the duration of ventricular fibrillation on defibrillation, the effects of ventricular fibrillation durations of 5, 15, and 30 seconds on the energy requirements for successful internal defibrillation were compared in 15 closed chest dogs with internal electrodes. The electrode configuration utilized a transvenous right heart catheter with two electrodes and a precordial subcutaneous patch electrode, with a single bidirectional pulse discharged between the distal catheter electrode and the proximal catheter and patch electrodes. Curves of energy vs. percentage of successful defibrillation were constructed and logistic regression was used to derive 90% and 50% successful energy doses (ED90 and ED50). The mean ventricular fibrillation activation interval just prior to defibrillation was determined from discrete RV endocardial electrograms. Four dogs died during testing, all because of inability to defibrillate after 30 s of ventricular fibrillation. In the remaining 11 dogs, the ED90 increased from (mean +/- SD) 27 +/- 13J at 5 s to 41 +/- 14J at 30 s (p less than .01). The mean ventricular fibrillation activation interval decreased from 107 +/- 21 ms at 5 s to 95 +/- 18 ms at 30 s (p less than .01). In conclusion, the energy required for internal defibrillation in dogs using this electrode configuration increases with longer durations of ventricular fibrillation, and is associated with more rapid ventricular fibrillation activation intervals.

Animals↗

PubMed1989

Estimating the duration of ventricular fibrillation.

As the duration of time between the onset of ventricular fibrillation and the application of defibrillation (downtime) increases, the rate of successful resuscitation decreases. Results of recent animal studies suggest that the rate of successful resuscitation may be increased after a prolonged cardiorespiratory arrest when pharmacologic therapy is instituted before defibrillation. An accurate estimation of downtime could be critical in selecting the most appropriate therapeutic intervention. The purpose of our study was to determine whether changes in the frequency or amplitude of the ventricular fibrillation ECG signal during cardiac arrest could be used to estimate downtime. We characterized the dynamics of both total power and frequency distribution of the power in the ECG during ventricular fibrillation in 11 swine to determine whether enough information existed in either parameter to estimate downtime. The median frequency of the power spectrum was used to track power distribution. Both parameters followed a dynamic, repeatable pattern. However, median frequency showed less intersubject variability than did total power. A mathematical model of median frequency was developed and used with data obtained from ten additional swine to estimate downtime. The model estimated downtime to within 1.3 minutes of actual downtime between one and ten minutes of ventricular fibrillation. Our study has identified a new, potentially useful parameter for studying various management strategies in ventricular fibrillation as a function of downtime.

Animals↗

PubMed2001

Isolated noncompaction of ventricular myocardium associated with fatal ventricular fibrillation.

A female infant with isolated noncompaction of ventricular myocardium who developed ventricular tachyarrhythmia is described. Wolff-Parkinson-White syndrome was shown by electrocardiography. At 9 months of age, the patient suddenly developed cardiac arrest. Electrocardiography following resuscitation with DC cardioversion demonstrated sinus rhythm without delta wave. The QT interval was normal. Frequent premature ventricular captures caused ventricular fibrillation. DC cardioversion was necessary to terminate frequent attacks of ventricular fibrillation until the introduction of beta blockers and lidocaine. Two-dimensional echocardiogram confirmed the diagnosis of isolated non-compaction of ventricular myocardium. Three months later, the patient died of ventricular fibrillation during respiratory syncytial viral infection.

Cardiomyopathies↗

PubMed1997

Calcium antagonists and prevention of ventricular fibrillation induced by transient or persistent ischemia.

Experimental studies have shown the limitation by calcium antagonists of the propensity to fibrillation secondary to the occlusion of a large coronary artery. However, this capacity, studied in the acute phase of infarction, is less obvious and still under debate. Ischemia was therefore produced in anesthetized, open-chest pigs by complete occlusion of the left anterior descending coronary artery according to two modes, either near its origin during brief but increasing periods (30, 60, 120, 180 s, etc) or half-way from this origin for a much longer time (60 min). The time course of vulnerability to fibrillation was monitored by ventricular fibrillation threshold (VFT), measured by trains of diastolic stimuli of 100 ms. Verapamil was administered in a 50 micrograms/kg dose followed by 2 micrograms/kg/min infusion. 1) In the case of brief proximal occlusions under pacing at a constant high rate (180 beats/min), verapamil slowed the decline of VFT from 6-8 mA to nearly 0 mA. VFT was 4.4 +/- 0.4 mA after 60 s ischemia, whereas it had already fallen to 1.8 +/- 0.3 mA (p < 0.001) in the absence of the drug. Accordingly, the onset of spontaneous fibrillation which depends on the decrease in VFT to about 0 mA was prolonged from 2-3 to 6-9 min. Bradycardia, concurrently produced by verapamil, is a factor which enhances these alterations. 2) In the case of a persistent midportion occlusion of the artery under sinus rate, fibrillations were similarly delayed by verapamil from 14-25 to 23-49 min after occlusion, but they were more numerous. VFT was lowered to critical values later, but also for a longer time. The period propitious to fibrillation was prolonged because the return of VFT to higher values reflecting hypoexcitability subsequent to the first cell injury was substantially delayed. Consequently, calcium antagonists should often prevent ventricular fibrillation when transient ischemia disappears before VFT falls to the vicinity of 0 mA. In contrast, a real benefit could not be expected from these drugs when ischemia is persistent since they then only delay fibrillations, the number of which is increased.

Analysis of Variance↗

PubMed2000

Prognostic implications of ventricular fibrillation in acute myocardial infarction: new strategies required for further mortality reduction.

OBJECTIVE: To determine the changing risk of ventricular fibrillation, the prognostic implications, and the potential long term prognostic benefit of earlier hospital admission, after acute myocardial infarction. DESIGN: Prospective observational study. SETTING: A district general hospital in east London. PATIENTS: 1225 consecutive patients admitted to a coronary care unit with acute myocardial infarction. MAIN OUTCOME MEASURES: Time of onset of pain and ventricular fibrillation, and long term survival of patients admitted with acute myocardial infarction. RESULTS: The rate of ventricular fibrillation in these hospital inpatients was high in the first hour from onset of pain (118 events/1000 persons/h; 95% confidence interval (CI) 50.7 to 231) and fell rapidly to an almost constant low level by six hours; 27.4% of patients with early ventricular fibrillation died in hospital, compared with 11.6% of those without (p < 0.0001), but mortality in patients who survived to hospital discharge was not altered by early ventricular fibrillation (five year survival: 75.0% (95% CI 60.0% to 84.8%) with ventricular fibrillation v 73.3% (95% CI 69.6% to 76.6%) without ventricular fibrillation). CONCLUSIONS: Patients successfully resuscitated from early ventricular fibrillation have the same prognosis as those without ventricular fibrillation after acute myocardial infarction. Faster access to facilities for resuscitation must be achieved if major improvements in the persistently high case fatality of patients after acute myocardial infarction are to be made.

Aged↗

PubMed1992

Intracellular calcium during pacing-induced ventricular fibrillation. Effects of lidocaine.

Hemodynamics and endocardial [Ca2+]i transients were studied during ventricular fibrillation in isolated perfused rat hearts. During 1 minute of pacing-induced ventricular fibrillation, the diastolic fibrillatory [Ca2+]i level increased significantly (p less than 0.001) above the end-systolic [Ca2+]i concentration of the last regular contraction. A bolus of lidocaine led to a decrease in the [Ca2+]i level during fibrillation (p less than 0.007) to the end-diastolic level of baseline conditions and then subsequently converted the heart to sinus rhythm. In 13 (62%) of the 21 studies described, post-lidocaine ventricular fibrillation converted to a brief period of asystole followed by sinus rhythm; in 8 (38%) of the studies, post-lidocaine ventricular fibrillation switched to ventricular tachycardia. Postfibrillatory cardiac dysfunction was related to the duration and degree of elevated diastolic [Ca2+]i. The authors conclude that [Ca2+]i levels are increased during ventricular fibrillation, and that lidocaine treatment leads to a prompt decrease in [Ca2+]i preceding conversion to sinus rhythm.

Animals↗