No abstract available.
Echocardiography ; Ventricular Fibrillation*

No abstract available.
Echocardiography ; Ventricular Fibrillation*

No abstract available.
Epilepsy ; Humans ; Seizures ; Ventricular Fibrillation

Profound hypothermia (15 degrees C) was induced in 36 mogrel dogs anesthetized with nitrous oxide-oxygen-d-tubocurarine. Prcpranolol (0.3 mg/kg) or MJ 1999(0.8 mg/kg) was administered intravenously 10 minutes prior to the start of cooling. Significant protection against ventricular fibrillation was provided by MJ 1999, but not by propranolol. With available evidence that hypothermia causes increased catecholamine release and that MJ 1999 is more specific in its beta-adrenergic blocking prcperties than propranolol, the authors findings suggest that ventricular fibrillation during hypothermia is due to beta-adrenergic hyperactivity.
Animals ; Dogs* ; Hypothermia* ; Propranolol* ; Sotalol* ; Ventricular Fibrillation*

The external defibrillator is an emergency instrument used very widely in clinics. It plays an important role in rescuing ventricle fibrillation (VF) patients. We have designed an external defibrillator using the truncated exponential biphasic waveform. The system consists of three parts: the ECG collection module, the control module and the defibrillator module. They are introduced respectively, listing the main problems and the methods to solve them. Some experiments have been done and the corresponding results are given.
Animals ; Defibrillators ; Equipment Design ; Swine ; Ventricular Fibrillation

Child ; Electrocardiography ; Humans ; Male ; Ventricular Fibrillation ; physiopathology

Defibrillators, Implantable ; Electric Countershock ; Humans ; Ventricular Fibrillation

PURPOSE: Therapeutic hypothermia has been recommended for postcardiac arrest coma due to ventricular fibrillation (Vf). However, although it is well known that the cardiac arrest due to non-Vf is associated with poorer neurologic outcome that Vf, there is no study that evaluates the effect of mild hypothermia on the cardiac arrests due to non-Vf. So, we intend whether mild hypothermia would improve the neurologic outcome of them saftly. METHODS: We retrospectively analyzed the patients with cardiac arrest due to asystole or pulseless electrical activity who was presented at hopsital and successfully showed the return of spontaneous circulation. We divided the patients to two groups according to implementation of hypothermia and statistically compared the complication and neurologic outcome at discharge. RESULTS: A total of sixty one patients were analyzed in this study. Baseline clinical and physiological characteristic were similar between patients treated with mild hypothermia or with conservative treatment. The complication rate did not differ significantly between the two groups. However, the good outcome at hospital discharge was observed in 13 of 41 patients treated with mild hypothermia compared with 0 of 27 patients treated with conservative treatment. CONCLUSION: Mild therapeutic hypothermia for the treatment of postcardiac arrest due to non-Vf can be saftly implemented with a major benefit on patient outcome.
Coma ; Heart Arrest ; Humans ; Hypothermia ; Resuscitation ; Retrospective Studies ; Ventricular Fibrillation

BACKGROUND: Several different patterns of wavebreak have been described by mapping of the tissue surface during fibrillation. However, it is not clear whether these surface patterns are caused by multiple distinct mechanisms or by a single mechanism. METHODS: To determine the mechanism by which wavebreaks are generated during ventricular fibrillation, we conducted optical mapping studies and single cell transmembrane potential recording in 6 isolated swine right ventricles. RESULTS: Among 763 episodes of wavebreak (0.75 times/sec/cm2), optical maps showed 3 patterns: 80% due to a wavefront encountering the refractory waveback of another wave, 11.5% due to wavefronts passing perpendicularly each other and 8.5% due to a new (target) wave arising just beyond the refractory tail of a previous wave. Computer simulations of scroll waves in 3-D tissue showed that these surface patterns could be attributed to two fundamental mechanisms: head-to-tail interactions and filament break. CONCLUSION: We conclude that during sustained ventricular fibrillation in swine RV, surface patterns of wavebreak are produced by two fundamental mechanisms: head-to-tail interaction between waves and filament break.
Computer Simulation ; Heart Ventricles* ; Membrane Potentials ; Swine* ; Ventricular Fibrillation*

BACKGROUND: It is known that QT dispersion represents asynchronous repolarization of ventricle which is related to ventricular fibrillation. The incidence of ventricular arrhythmia is increased after acute myocardial infarction. So this study compared QT dispersion and other repolarization indexes for detection of asynchronous repolarization in acute myocardial infarction. We also investigated which portion of repolarization is the key portion of the asynchrony. METHODS: In 37 acute myocardial infarction patients and 38 angina patients dispersion of QT, JT, JTpeak and QTpeak were measured. We also measured maximum adjacent dispersion of same parameters in precordial leads. In 20 survived patients and 17 dead patients after acute myocardial infarction were also compared. We also investigated correlation of PVC's on Holter monitoring with these repolarization parameters. RESULTS: 1) All ventricular repolarization indexes(QT, QTc, JT, JTpeak, QT peak and TpeakTend dispersion) were significantly increased in acute myocardial infarction group than compared with those of angina group(p<0.05). 2) Maximal precordial dispersion(QT, QTc, JT, JTpeak and QTpeak) were also significantly increased in acute myocardial infarction group than angina group(p<0.05). 3) Dead patient group after myocardial infarction showed significantly increased QTc and TpeskTend dispersion compared with those of survived patient group(p<0.05). 4) Multivariate linear correlation showed that TpeakTend dispersion and JT dispersion was correlated with QT dispersion. CONCLUSIONS: There were asynchronous myocardial repolarization changes in acute myocardial infarction. Our study demonstrated that T wave change was major determinant of dispersion of myocardial repolarization.
Arrhythmias, Cardiac ; Electrocardiography, Ambulatory ; Humans ; Incidence ; Myocardial Infarction* ; Ventricular Fibrillation