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PubMed1999

Electrical restitution and spatiotemporal organization during ventricular fibrillation.

Despite recent advances in our understanding of the mechanism for ventricular fibrillation (VF), important electrophysiological aspects of the development of VF still are poorly defined. It has been suggested that the onset of VF involves the disintegration of a single spiral wave into many self-perpetuating waves. It has been further suggested that such a process requires that the slope of the electrical restitution relation be >/=1. The same theory anticipates that a single spiral wave will be stable (not disintegrate) if the maximum slope of the restitution relation is <1. We have shown previously that the slope of the restitution relation during rapid pacing and during VF is >/=1 in canine ventricle. We now show that drugs that reduce the slope of the restitution relation (diacetyl monoxime and verapamil) prevent the induction of VF and convert existing VF into a periodic rhythm. In contrast, a drug that does not reduce the slope of the restitution relation (procainamide) does not prevent the induction of VF, nor does it regularize VF. These results indicate that the kinetics of electrical restitution is a key determinant of VF. Moreover, they suggest novel approaches to preventing the induction or maintenance of VF.

Action Potentials↗

PubMed1983

Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation.

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.

Aged↗

PubMed2000

Ventricular fibrillation exhibits dynamical properties and self-similarity.

Electrocardiographic recordings of ventricular fibrillation (VF) appear chaotic. Previous attempts to characterize the chaotic nature of VF have relied on peak-to-peak intervals [Witkowski et al., Phys. Rev. Lett. 1995;75(6):1230-3; Garfinkel et al., J. Clin. Investig. 1997;99(2):305-314; Hastings et al., Proc. Natl. Acad. Sci. USA 1996;93:10495-9], the frequency spectrum [Goldberger et al., 1986;19:282-289] or other derived measures [Kaplan and Cohen, Circ. Res. 1990;67:886-92], with results that demonstrate some characteristics of chaos. We have sought to determine whether VF is chaotic rather than random and whether the waveform can be described quantitatively using the tools of fractal geometry. We have constructed an attractor, measured the correlation dimensions, estimated the embedding dimension and measured Lyapunov exponents. When the digitized waveform is analyzed directly, VF exhibits nonrandom, chaotic behavior over a decade of sampling frequency. Within the scaling range we have estimated the Hurst exponent, and the self-similarity dimension of the VF waveform, supporting the presence of chaotic dynamics. Furthermore, these characteristics are measurable in a porcine model of VF under different recording conditions, and in VF recordings taken from human subjects immediately prior to defibrillation. Analyses of the Hurst exponents and self-similarity dimensions are correlated with the duration of VF, which may have clinical applications.

Animals↗

PubMed1990

Flecainide: long-term effects in patients with sustained ventricular tachycardia or ventricular fibrillation.

Efficacy of flecainide was investigated in 50 patients with sustained ventricular tachycardia (n = 38) or ventricular fibrillation (n = 12) during a 4-week in-hospital and 1-year follow-up period. Furthermore, the predictive value of programmed electrical stimulation, Holter monitoring, and exercise testing on outcome of long-term treatment was studied. Etiology of the tachyarrhythmia was coronary artery disease in 37 patients and other etiologies in 13 patients. The success rate of flecainide after 1 year, based on intention to treat, was 54%. The success rate during the in-hospital phase was 84% (in six patients flecainide was discontinued because of tachyarrhythmia and in two because of side effects). Calculated after 4 weeks hospitalization, the success rate was 78% for patients with tachyarrhythmias based on coronary artery disease and 55% for patients with tachyarrhythmias based on other etiologies (11 patients showed recurrences and two patients severe side effects). Patients with tachyarrhythmias based on coronary artery disease showed a lower ejection fraction and earlier recurrence than patients with arrhythmias based on other etiologies. Proarrhythmic effects developed in six patients (12%). Electrophysiological evaluation was performed in 28 patients at baseline and after intravenous flecainide. Negative predictive value of the electrophysiological evaluation after intravenous flecainide for patients with inducible tachyarrhythmias at baseline (n = 21) was 40%. For Holter monitoring (n = 24) this value was 86%. Non-ischemia-related induction of tachycardia by exercise was present in two of 30 patients on flecainide; both patients showed recurrence of the tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1994

Ventricular fibrillation voltage as a monitor of the effectiveness of cardiopulmonary resuscitation.

Ventricular fibrillation (VF) voltage was previously identified as a predictor of the success of cardiopulmonary resuscitation. In the present study we investigated the mechanism by which VF voltage predicts the success of cardiac resuscitation in a well-established rodent model of cardiac arrest. After 4 minutes of untreated VF, precordial compression was initiated and maintained for 6 minutes. Increases in coronary perfusion pressure during precordial compression were associated with concomitant increases in VF voltage (r = 0.61, p = 0.013). Significantly greater coronary perfusion pressure (24 vs 17 mm Hg) and VF voltage (0.17 vs 0.12 mV) were observed in resuscitated animals. To obviate electrical artifacts produced by precordial compression, boluses of oxygenated blood were injected into the ascending aorta in another 5 animals as an alternative method of cardiac resuscitation. This restored myocardial perfusion before defibrillation. Increases in VF voltage from 0.04 mV to 0.47 mV during aortic infusions were again correlated with coronary perfusion pressure (r = 0.62, p < 0.01) and predicted the success of cardiac resuscitation. Greater VF voltages after initiation of cardiac resuscitation were associated with increases in myocardial creatine phosphate, from 0.23 to 0.70 mmol/kg wet weight, and significant decreases in lactate content, from 22.8 to 13.9 mmol/kg wet weight. Increases in creatine phosphate were highly correlated with increases in VF voltage (r = 0.99, p < 0.01). Accordingly, increases in VF voltage during cardiac resuscitation reflect increases in myocardial perfusion and favorable changes in myocardial energy metabolism. As such, VF voltage, like coronary perfusion pressure, serves as a quantitative predictor of the success of cardiopulmonary resuscitation.

Action Potentials↗

PubMed1990

Prognosis of late versus early ventricular fibrillation in acute myocardial infarction.

To determine the prognosis of late ventricular fibrillation (VF) after acute myocardial infarction (AMI), the length of the monitoring period after AMI was extended. All patients in this series were continuously monitored in a coronary care unit to ensure observation of all VF within 18 days of AMI. From 1977 to 1985, 4,269 patients were admitted with AMI and 413 (9.6%) had in-hospital VF. Of these 281 (6.8%) had early VF (less than 48 hours after AMI) and 132 (3.2%) had late VF (greater than or equal to 48 hours after AMI). In-hospital mortality was 50 and 54% for early and late VF, respectively (p = 0.31). Kaplan-Meier survival analysis showed better survival after discharge for patients with early versus late VF (p = 0.009) but this difference was fully explained by the presence of heart failure. Survival analysis showed the same prognosis after 1, 3 and 5 years for early and late VF, when VF was not associated with heart failure. When VF was associated with heart failure (secondary VF) early VF had a greater mortality than late VF after 2 and 5 years. Logistic regression analysis showed that heart failure (relative risk 1.9 [1.1 to 3.1]) and cardiogenic shock (relative risk 3.9 [1.8 to 8.5]) were significant risk factors for in-hospital death. Late VF compared to early VF had no prognostic implication (relative risk 1.0 [0.6 to 1.6]). For patients discharged from the hospital, risk factors were heart failure (1.8 [1.1 to 2.8]) and previous AMI (1.6 [1.3 to 2.1]).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation.

The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1-10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After beta-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without beta-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after beta-blockade. We conclude that a burst of 15-30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. beta-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.

Adrenergic Uptake Inhibitors↗

PubMed1992

Contrasting effects of cyclic AMP increase caused by beta-adrenergic stimulation or by adenylate cyclase activation on ventricular fibrillation threshold of isolated rat heart.

Increased myocardial tissue cyclic AMP has been associated with both a positive inotropic and a proarrhythmic effect. We wished to determine whether two agents that increase myocardial cyclic AMP levels by different mechanisms would induce comparable changes in vulnerability of the heart to ventricular fibrillation (VF) and in the inotropic status. Using an isolated perfused rat heart model, we studied the effects of beta-adrenoceptor stimulation by isoproterenol (ISO) and direct activation of adenylate cyclase by forskolin. The ventricular fibrillation threshold (VFT) was taken as an index of the vulnerability to VF and peak left ventricular systolic pressure (LVSP) as a measure of the force of LV contraction. ISO resulted in a dose-related increase in tissue cyclic AMP with a corresponding decrease in VFT and a marked increase in LVSP. Forskolin produced a delayed but exponential increase in cyclic AMP at concentrations greater than 3 x 10(-7) M with relatively small increases in LVSP. With forskolin, the VFT decreased only at extremely high cyclic AMP levels, suggesting that the drug had increased cyclic AMP in a compartmentalized manner. The discrepant effects of ISO and forskolin on VFT could not be explained by changes in heart rate (HR). These results show that an increase in tissue cyclic AMP can have markedly different arrhythmogenic effects depending on the mechanism by which cyclic AMP is increased.

Adenylyl Cyclases↗

PubMed1983

Reduced human ventricular fibrillation threshold associated with contrast-induced Q-T prolongation.

Injection of contrast dye during selective coronary arteriography prolongs the Q-T interval well beyond that expected for the accompanying bradycardia. A case is presented in which a 5 mA stimulus delivered prematurely by an improperly sensing ventricular demand pacemaker initiated ventricular fibrillation during coronary arteriography, although no evidence of coronary or other cardiac disease was found. An analysis is made of the progressive Q-T and T changes following contrast dye injection, and their relation to the onset of ventricular fibrillation. The implications of these observations are discussed in light of existing data on human ventricular vulnerability.

Aged↗

PubMed1991

Ventricular fibrillation during transesophageal atrial pacing in an infant with Wolff-Parkinson-White syndrome.

A complication of transesophageal atrial pacing in an infant with Wolff-Parkinson-White syndrome (WPW) is reported. A newborn infant born with fetal hydrops had recurrent supraventricular tachycardia (SVT) that required repeated successful conversion by transesophageal atrial pacing. Because of secondary left ventricular dysfunction, digoxin was administered. During repeat transesophageal atrial pacing for recurrent SVT, ventricular fibrillation occurred. Although it is unclear which of several possible contributing factors was responsible for the ventricular fibrillation, recommendations are appropriate to minimize the risk in infants with WPW.

Cardiac Pacing, Artificial↗

PubMed1984

Treatment of prehospital refractory ventricular fibrillation with bretylium tosylate.

Among 218 patients treated for prehospital arrest during an eight-month baseline period prior to addition of bretylium tosylate to the paramedic protocol in Columbus, 16 (7.3%) were seen with refractory ventricular fibrillation (RVF). These patients failed to respond to multiple countershocks, lidocaine, bicarbonate and epinephrine, and either were transported in arrest during cardiopulmonary resuscitation (CPR)(14) or were pronounced dead at the scene (2). A single patient was eventually resuscitated in and discharged from the hospital. During the subsequent 16 1/2-month experience with bretylium used only for prehospital RVF, 421 patients with prehospital arrest were seen, 35 of whom (8.3%) had RVF. All but five patients were defibrillated successfully, and 14 (40%) were converted to a rhythm sufficient to obviate CPR during transportation. Eleven patients (31%) survived to be admitted to the hospital, and eight of 35 (23% vs 1/16 or 6.2% above, P less than .05) were discharged and remained well three to 17 months later. Bretylium tosylate may provide life-saving therapy for refractory prehospital ventricular fibrillation so that survival from an almost uniformly fatal condition is improved. While patients with persistent arrest generally should be transported to the hospital, such patients should not be subjected to the difficulties of CPR in transit unless they are first given bretylium if RVF is present.

Bretylium Compounds↗

PubMed1979

Concentration of myocardial cyclic AMP and ventricular fibrillation induced by aminophylline.

The concentration of myocardial cyclic AMP was measured in 9 dogs by radioimmunoassay after the administration of aminophylline. Fourteen dogs served as control. The concentration of cyclic AMP in the left ventricle was the highest and the lowest value was obtained in the right atrium in the control dogs. Ventricular fibrillations were induced immediately after the injection of 30 mg/Kg aminophylline in 3 dogs out of 9. The concentration of the left ventricular cyclic AMP in 6 dogs which tolerated aminophylline was significantly elevated compared with that of the control dogs (p less than 0.05). The left ventricular cyclic AMP in 3 dogs with ventricular fibrillation was significantly higher compared with that in the aminophylline tolerated dogs with non-fibrillating hearts (p less than 0.01). These results showed that the concentration of cyclic AMP was elevated in the fibrillating heart.

Aminophylline↗

PubMed1999

Ultrasound detection of ventricular fibrillation disguised as asystole.

Ultrasonography in the emergency department is being used for many purposes, including the evaluation of patients with cardiac arrest. Ultrasound testing has been shown to be useful in such patients in determining the presence of true electromechanical dissociation and pericardial effusions. We report a case of ventricular fibrillation identified by ultrasonography that appeared as asystole on ECG monitoring. Recognition of this ultrasound application can aid in the prompt diagnosis of occult ventricular fibrillation and allow for proper treatment with defibrillation.

Aged↗

PubMed2002

Transthoracic defibrillation of short-lasting ventricular fibrillation: a randomised trial for comparison of the efficacy of low-energy biphasic rectilinear and monophasic damped sine shocks.

BACKGROUND: Biphasic rectilinear shocks are more effective than monophasic shocks for transthoracic atrial defibrillation and for ventricular arrhythmias during electrophysiological testing. We undertook the present study to compare the efficacy of 100 J rectilinear biphasic waveform shocks with 150 J monophasic damped sine waveform shocks for transthoracic defibrillation of true ventricular fibrillation during defibrillation threshold testing (DFT). The second aim of the study was to analyse the influence of patch positions on the efficacy of defibrillation. METHODS: 50 episodes of 14 patients (age ranging from 37 to 82 years) who underwent DFT testing were randomised for back-up shocks with either a sequence of 100 and 200 J biphasic waveform, or a sequence of 150 and 360 J conventional monophasic shocks. A binary search protocol was used at implantation and before hospital discharge. Patients were also randomised to an anteroposterior position versus a right-anterior-apical position. A crossover was performed between implantation and pre-hospital discharge for biphasic versus monophasic sequence as well as for the 2 different positions. RESULTS: After failed internal shocks, 27 episodes were treated with biphasic, and 23 with monophasic shocks. The first attempt by the external device did not terminate II episodes (2 biphasic, 9 monophasic). The first shock efficacy was significantly greater with biphasic than with monophasic shocks (p < 0.02). The overall success rate was 93% with biphasic shocks and 64% with monophasic shocks. In multivariate regression analysis including patch position, arrhythmia duration, type of waveform, testing order and session, only waveform was associated with successful defibrillation (p < 0.02). CONCLUSION: For transthoracic defibrillation of ventricular fibrillation, low-energy rectilinear biphasic shocks are more effective than monophasic shocks. The position of the defibrillation shock pads has no influence on the biphasic shock efficacy, but anteroposterior pad position is more effective using monophasic shocks.

Adult↗

PubMed1997

Effects of myocardial ischemia on ventricular fibrillation inducibility and defibrillation efficacy.

OBJECTIVES: This study investigated the effects of acute global ischemia on the vulnerable window, the upper limit of vulnerability and the defibrillation threshold. BACKGROUND: Myocardial ischemia, an important factor for arrhythmogenesis and sudden death, may affect the inducibility of ventricular fibrillation by T wave shocks as well as the defibrillation threshold. However, studies of the effect of ischemia on the defibrillation threshold remain inconclusive, and the effect of ischemia on recently established variables of ventricular fibrillation vulnerability is still unknown. METHODS: Ten isolated, perfused rabbit hearts were immersed in a tissue bath between two shock plate electrodes. Truncated 5-ms biphasic shocks were used to determine the vulnerable window, the upper limit of vulnerability and the defibrillation threshold. Measurements were performed during baseline and at 10 to 15 min of acute ischemia induced by an 80% reduction of coronary flow. The effects of ischemia were monitored by measuring the dispersion of ventricular activation and repolarization using multiple monophasic action potential recordings. RESULTS: Acute ischemia caused an increase in dispersion of activation (baseline vs. ischemia [mean +/- SD]: 22 +/- 6 vs. 34 +/- 10 ms, p < 0.001) and dispersion of repolarization (37 +/- 16 vs. 69 +/- 29 ms, p < 0.01). The width of the vulnerable window increased from 25 +/- 22 ms during baseline to 75 +/- 26 ms during ischemia (p = 0.001). The upper limit of vulnerability (baseline vs. ischemia: 294 +/- 44 vs. 274 +/- 53 V, p = 0.21) and the defibrillation threshold (271 +/- 33 vs. 268 +/- 42 V, p = 0.74) remained unchanged during ischemia. CONCLUSIONS: Acute global ischemia caused a threefold increase in the width of the vulnerable window. This increase was associated with increased heterogeneity of ventricular activation and repolarization. Despite these marked changes, the upper limit of vulnerability and the defibrillation threshold were not affected by acute myocardial ischemia. Thus, the previously reported similarity between both measures was maintained under these adverse conditions.

Action Potentials↗

PubMed1989

Autonomic response to coronary occlusion in animals susceptible to ventricular fibrillation.

Disturbances in autonomic control during myocardial ischemia may contribute significantly to the development of malignant cardiac arrhythmias. Therefore acute ischemia was induced in 29 mongrel dogs with healed myocardial infarctions during an exercise test. Seventeen animals developed ventricular fibrillation (susceptible, S), whereas 12 dogs did not (resistant, R). Before the exercise plus ischemia test a coronary occlusion was made at rest. The amplitude of respiratory sinus arrhythmia (0.24- to 1.04-Hz component of R-R interval fluctuation) was used as an index of cardiac vagal tone. Acute ischemia elicited a significantly larger heart rate increase in susceptible animals (S: control 115.6 +/- 0.8, occlusion 176.4 +/- 8.2 beats/min vs. R: control 114.6 +/- 8.9, occlusion 145.7 +/- 7.5 beats/min). Accompanying the heart rate increase were significantly greater reductions in the cardiac vagal tone index in the susceptible animals. (S: control 6.4 +/- 0.3, occlusion 2.2 +/- 0.6 ln ms2 vs. R: control 6.6 +/- 0.4, occlusion 5.1 +/- 0.5 ln ms2). beta-Adrenergic receptor blockade reduced the heart rate increases but exacerbated the reductions in the cardiac vagal tone index. These data suggest that coronary artery occlusion elicits a significantly greater increase in sympathetic activity coupled with a greater reduction in parasympathetic activity in animals subsequently shown to be susceptible to ventricular fibrillation.

Animals↗

PubMed1985

[Electrocardiostimulation in the treatment of recurrent ventricular fibrillation in a patient with long QT syndrome on the ECG].

Electrical stimulation of the ventricles with frequency more than spontaneous heart rate was used in a 36-year old patient suffering from rheumatic fever, paroxysms of ciliary arrhythmia to prevent recurring ventricular fibrillation in the presence of a QT elongated interval on the ECG. Medicinal therapy was provided in parallel. She was discharged in a satisfactory condition. For 11 mos. of outpatient treatment there were no fits of loss of consciousness; the QT interval was not elongated. It is concluded that electrocardiostimulation is effective for the prevention of ventricular fibrillation in patients with the syndrome of a QT elongated interval on the ECG.

Adult↗

PubMed1983

Physical training increases ventricular fibrillation thresholds of isolated rat hearts during normoxia, hypoxia and regional ischemia.

The effect of exercise training on cardiovascular mortality is controversial. The purpose of this study was to determine the effect of a period of treadmill training on the ventricular fibrillation threshold of the isolated rat heart. Trained hearts had higher threshold values during standard, control perfusion conditions, and when exposed to hypoxia, hypoxia plus isoproterenol infusion, or when subjected to coronary artery ligation. Myocardial metabolic studies failed to define the mechanism for the effect of running training. However, in coronary ligated hearts, the content of the arrhythmogenic substance 3',5' cyclic adenosine monophosphate (cyclic AMP) was reduced in the ischemic zone of hearts from trained rats. Cyclic AMP levels were also lower in trained hearts during control perfusions. We conclude that running training increases the resistance of the heart to ventricular fibrillation by mechanisms that are largely unknown, although they may involve cyclic AMP.

Animals↗