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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrical activity of the heart was studied in acute, subacute and chronic benzene, toluene and xylene poisoning by means of NEK-2 type apparatus in CFY male rats. In the early period of acute intoxication benzene and its methyl derivatives, injected either intraperitoneally or subcutaneously or administered by inhalation did not cause changes in the ECG. Intravenously injected toluene induced a rapid and permanent decrease in blood pressure, in higher doses respiratory paralysis. In acute inhalation toluene and xylene poisoning the anesthesia was followed by respiratory paralysis, bradyarrhythmia and asystole, while inhalation of benzene induced respiratory paralysis followed by ventricular fibrillation. Subacute poisoning with benzene, toluene and xylene caused disorders in repolarization and arrhythmia. The degree, incidence and development of these phenomena depended on the dose and the duration of exposure. The effect of benzene influencing ECG was appreciably more intensive than that of toluene or xylene. Owing to the high number of spontaneous ECG changes due to ageing, it is difficult to evaluate the effect of chronic exposure to the agents under investigation.
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PMID:ECG changes in benzene, toluene and xylene poisoned rats. 103 54

During the acute phase of myocardial infarction, two groups of patients are observed. Patients in the first group have no significant complications, and approximately 95 per cent of these patients recover fully without any specific therapy. Patients in the second group may have various complications, some of which are benign, whereas others may lead to a fatal outcome. The complications may be divided into four major types: 1. Cardiac arrhythmias and conduction defects. The tachyarrhythmias and bradyarrhythmias are the most frequently encountered complications in patients with acute myocardial infarction. Tachyarrhythmias include ventricular premature beats, ventricular tachycardia, ventricular fibrillation, supraventricular tachycardia, atrial flutter, and atrial fibrillation. Bradyarrhythmias include sinus and junctional bradycardia and various degrees of heart block. Those patients who are unable to reach a hospital and die suddenly presumably succumb to ventricular fibrillation. 2. Left ventricular failure and cardiogenic shock. In more than 33 per cent of patients with acute myocardial infarction, a third heart sound and pulmonary rales may be heard. If they are present for only 24 hours, the physical findings may indicate an alteration of left ventricular failure. However, if they persist for a few days and disappear after medical therapy, mild left ventricular failure may be present. About 12 per cent of patients have acute pulmonary edema, and 10 per cent of patients develop cardiogenic shock. These two complications carry a high mortality rate (40 per cent and nearly 100 per cent respectively). 3. Rupture of the heart. Cardiac rupture may occur in the free wall, ventricular septum, and papillary muscles. These complications, although less frequently encountered, cause a number of deaths in patients with acute myocardial infarction. 4. Thromboembolism. Under this category are included pulmonary embolism, systemic arterial embolism, and systemic venous thrombosis.
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PMID:The acute phase of myocardial infarction. 110 71

The current widespread interest in early (pre-hospital) coronary care has raised questions regarding the safety and efficacy of the use of atropine in these circumstances. Although reports from early coronary care systems have been favorable, serious questions of safety have been raised on the basis of experimental animal studies and isolated case reports. A sample of the experience of a large scale emergency coronary care system in Columbus, Ohio has therefore been reviewed. A group of 70 patients who, during the early phases of myocardial infarction, exhibited bradyarrhythmia (less than 60 beats/min) was identified. When this group was further categorized on the basis of arterial pressure at the time of initial observation, patients with normal or elevated blood pressure had low mortality rates whether treated with atropine or not. In patients with hypotension the mortality rate was 75 percent without therapy, and 25 percent with therapy. Indeed, when normal hemodynamics were restored, the mortality rate was only 11 percent. Unexpected ventricular fibrillation occurred in 1 of 45 treated patients and 2 of 25 untreated patients. Although the study was not controlled, the data strongly suggest that atropine is both beneficial and safe for use in treating bradyarrhythmia and hypotension in the early phase of acute myocardial infarction.
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PMID:Beneficial effects of atropine in the pre-hospital phase of coronary care. 124 35

For obtaining the preliminary data on the pathogenesis of sudden death in calves naturally heavily infected with Strongyloides papillosus, we monitored 8 Holstein calves experimentally infected with the larvae on electrocardiographic and pneumographic changes. Six calves died suddenly on days 11 to 17 after infection. Sinus tachycardia had been recorded continuously since 1 to 6 days before death. Heart rates increased gradually until death. Since 1 or 2 days before death, various patterns of tachyarrhythmia and bradyarrhythmia had been observed among patterns of sinus tachycardia. Arrhythmias included serious ventricular premature beat, paroxysmal ventricular tachycardia, complete atrioventricular block and so on. The terminal pattern observed suddenly in all of the cases was ventricular arrhythmias consisting of serial ventricular tachycardia, flutter and fibrillation, which were followed by respiratory arrest. Abnormal pneumograms were not obtained before the terminal ventricular fibrillation. Two of 8 calves recovered from the infection, only one of which showed sinus arrest and the second degree of atrioventricular block transiently. We concluded that calves heavily infected with the larvae died due to sudden cardiac arrest.
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PMID:Sudden cardiac death in calves with experimental heavy infection of Strongyloides papillosus. 147 64

Ventricular arrhythmias are a frequent complication of myocardial infarction. In either the acute or the late stage, ventricular tachycardia and ventricular fibrillation represent the most common cause of cardiac death. About 15% of the patients with acute myocardial infarction die before entering the hospital, the majority due to ventricular fibrillation. Another 10 to 15% of the survivors of an acute myocardial infarction die suddenly within the subsequent year, again mostly due to ventricular arrhythmias. Independent risk factors for sudden cardiac death consist of depressed left ventricular function, persistent electrical instability (e.g. repetitive and complex VPB's, documented 'late potentials', inducibility of arrhythmias at programmed electrical stimulation), new onset complete-bundle branch block and large aneurysm of the left anterior ventricular wall. Bradyarrhythmias (i.e. high-degree AV-Block, asystole) are a far less common etiology of sudden cardiac death caused by an ischemic lesion to the conduction system. Betablockers have a well-known benefit in secondary prevention, whereas antiarrhythmic agents (with the exception of amiodarone) are ineffective in asymptomatic patients or may even increase the risk for sudden death due to a proarrhythmic effect (class IC); therefore, the latter are not recommended in asymptomatic patients with documented VPB's and preserved left ventricular function. The prognosis of patients with sustained VT and VF is poor. Their outcome is improved in responders to an individual antiarrhythmic therapy with serial drug testing or with subendocardial resection of localized areas and by implantation of a cardioverter defibrillator.
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PMID:[Rhythm disorders and infarction]. 168 95

In order to reduce the high mortality from ischemic heart disease, a mobile coronary care unit manned by a cardiologist has been operating in Florence since 1979. From 1980 to 1989 there were 13,029 interventions, 8,718 (66.9%) of which were cardiac emergencies. 1,718 (19.7%) patients showed acute myocardial infarction while in 2,274 angina was diagnosed (26.1%). Acute pulmonary edema and paroxysmal supraventricular tachyarrhythmias accounted, respectively, for 6.2% and 18.3% of total cardiac emergencies; moreover there were 753 (5.8%) attempted resuscitations in sudden cardiorespiratory arrest from cardiac causes. In acute myocardial infarction, the median time between the onset of symptoms and mobile coronary care unit arrival was 85 minutes, and 69.9% of patients were reached within 3 hours from the onset of symptoms. Ventricular fibrillation, ventricular tachycardia and asystole were observed respectively in 80 (4.6%), 42 (2.4%) and 50 (2.9%) patients. Success rate of emergency treatment was 81.3% for ventricular fibrillation, 88.1% for ventricular tachycardia and 18% for asystole. Prehospital mortality was 4.06%. The ECG picture of the 753 patients found in cardiac arrest showed sustained ventricular tachycardia in 12 (1.6%), ventricular fibrillation in 198 (26.3%), bradyarrhythmia in 28 (3.7%), and asystole in 431 (57.2%). Cardiopulmonary resuscitation was successfully performed in 230 patients (30.5%). Finally, more than 50% of the patients with angina, 20% of the patients with acute pulmonary edema, and 70% of the patients with paroxysmal supraventricular tachyarrhythmia were adequately treated at home and needed no hospitalization. The ten years experience of Florence Mobile Coronary Care Unit suggests that a community wide emergency cardiac care system can significantly reduce the pre-hospital mortality and the time delays preceding thrombolysis and intensive care in acute myocardial infarction. Moreover, the cardiac "sudden death" can often be successfully treated. Most other cardiac emergencies may be adequately treated at home and unnecessary hospitalizations can be avoided.
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PMID:[The mobile coronary unit of Florence: an evaluation of 10 years of prehospital cardiac care]. 186 89

Bradyarrhythmia or asystole is the most common rhythm disturbance with ventricular fibrillation and tachycardia, for 30-40% of patients admitted in intensive coronary care units. Already use in the therapy of bradyarrhythmia or asystole, as a method of emergency, immediately in place, the external pacing is very useful in an out of hospital therapy with personnel skilled in its use until the initiation of support therapy in coronary care units. Actually, with less significant side effects (no severe pain, no strong muscular contractions, no skin burns) and a best innocuity and tolerance based on the employment of larger adhesive pre-gelled patches, temporary transcutaneous cardiac stimulation is not only confined to unconscious patients but also in case of severe bradycardia, complete AV block in conscious patients. Our hemodynamic study shows a good level of systemic pressure and of cardiac index to permit the transport of patients in coronary care units in good conditions. Furthermore, the experimental study demonstrates the importance of the polarity of the electrodes and of the duration of the stimulus (more than 10 ms) to minimize the threshold (mA/cm2) so as to increase the tolerance in clinical application. Transcutaneous cardiac pacing is a simple and rapid pacing procedure with effective hemodynamic results for victims of out-of-hospital cardiac arrest and can be easily used in conscious patients without any complication.
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PMID:[Then hemodynamic efficacy of transcutaneous cardiac stimulation]. 209 64

An analysis has been made of long-term ECG recordings in 11 patients, 9 men and 2 women, mean age 69 +/- 7 years, who were carrying ECG recording equipment at the time of sudden death. Nine patients had coronary heart disease, one patient a dilatative cardiomyopathy and another one a combined aortic valve defect. Seven patients had a history of syncope. All patients had signs of cardiac insufficiency (NYHA index 3.0 +/- 0.6, heart-thorax quotient 0.55 +/- 0.05). Sudden death occurred predominantly whilst resting. In one patient it was due to bradyarrhythmia, in 10 to tachyarrhythmia, mostly ventricular tachycardia (initial heart rate 198 +/- 43/min; n = 8) which degenerated into ventricular fibrillation. Atrial fibrillation was present in 8 patients at the time of sudden death. Premonitory warning arrhythmias were not consistently detectable: comparison of arrhythmias in the first and last hour showed significant increases only in single ventricular extrasystoles (135 vs. 278 VES/h, P less than 0.05), not however in repetitive arrhythmias. An R-on-T phenomenon, as trigger mechanism of ventricular tachycardia, occurred in 5 cases. A synopsis of the published reports on approximately 110 patients with sudden death during long-term electrocardiographic monitoring confirmed that acute death is caused by bradyarrhythmias in approximately 15% (17 patients), and by tachyarrhythmias in 85% (94 patients). An increase in ventricular arrhythmias in the hour prior to death was observed in about 50% of patients and the R-on-T phenomenon, as the initiating mechanism for ventricular tachycardia, in 42%.
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PMID:[Sudden cardiac death in long-term electrocardiography]. 241 Feb 15

Much remains unknown about the conditions surrounding the occurrence of prehospital sudden cardiac arrest. We have investigated the clinical characteristics and predictors of survival in a total of 90 consecutive patients in whom sudden cardiac arrest (SCA) happened to occur during their hospitalization in general wards over the past 19 years. The types of arrhythmia present at the time of SCA were ventricular fibrillation (in 46% of cases), ventricular tachycardia (19%), and bradyarrhythmia (35%). The underlying causes were coronary artery disease (45%), cardiomyopathy (20%), and valvular disease (14%). SCA showed a circadian pattern, with many cases during the day and few at night. Prodromal symptoms included chest pain (16% of patients), dyspnea (11%) and palpitations (2%). Of the total of 90 subjects, 26 (29%) were discharged from hospital alive, and SCA recurred in 24% of these. The 5-year survival rate was 52%. The most important predictors of survival examined were initiation of cardiopulmonary resuscitation, NYHA class, and time of SCA. Of those in whom cardiopulmonary resuscitation was initiated within 1 min, 52% were discharged alive, but all of those not receiving it within 10 min died.
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PMID:Sudden cardiac arrest: clinical characteristics and predictors of survival. 263 23

In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed by a rescue shock of 40 A. In ventricular fibrillation episodes requiring rescue shocks, nine of 19 episodes (47%) exhibited second- or third-degree atrioventricular block at 15 seconds postdefibrillation compared with only one of 16 BW-A1433U episodes (6%). In protocol 2, the effect of BW-A1433U was determined in the presence of dipyridamole, a nucleoside uptake blocker known to potentiate the cardiac actions of adenosine. To counter the hypotensive effect of dipyridamole, methoxamine was continuously infused at 0.015 mg/kg/min i.v. Sequential episodes of ventricular fibrillation lasting 45 seconds were terminated by shocks of 40 A in the presence of methoxamine alone, after dipyridamole (1.5-7.5 mg i.v.), and after BW-A1433U (5 mg/kg i.v.). Over the first 15 seconds postdefibrillation, BW-A1433U significantly (p less than 0.05) increased the number of spontaneous beats (31 +/- 2) and systolic/diastolic blood pressure (111 +/- 4/67 +/- 5 mm Hg; mean +/- SEM; n = 9) compared with both methoxamine (16 +/- 2 beats; 98 +/- 14/52 +/- 12 mm Hg; n = 5) and dipyridamole (8 +/- 3 beats; 58 +/- 11/27 +/- 6 mm Hg; n = 9), respectively. Rapid infusion of BW-A1433U during dipyridamole postdefibrillation periods raised heart rate and blood pressure to preventricular fibrillation levels within 30 seconds. Thus, BW-A1433U can reverse and prevent postdefibrillation bradyarrhythmia and hemodynamic depression. Endogenous adenosine may be an important mediator of postdefibrillation cardiovascular collapse.
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PMID:Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression. 273 45


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