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Fibrillation, ventricular

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. [Pg.180]

Barium metal and most barium compounds are highly poisonous. A notable exception is barium sulfate which is nontoxic because of its extreme iasolubihty ia water. Barium ion acts as a muscle stimulant and can cause death through ventricular fibrillation of the heart. Therefore, care must be taken to avoid contact with open areas of the skin. Workers must wear respirators (of type approved for toxic airborne particles), goggles, gloves, and protective clothing at all times. The toxic barium aluminate residue obtained from barium production is detoxified by reaction with a solution of ferrous sulfate and converted iato nontoxic barium sulfate. According to OSHA standards, the TWA value for Ba and Ba compounds ia air is 0.5 mg/m. ... [Pg.473]

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). [Pg.110]

Reentry mechanism Intranodal (AV node) reentry Extranodal reentry Reentrant tachyarrhythmia Atrial flutter Atrial fibrillation Ventricular tachycardia Ventricular fibrillation Conduction B/ocks ... [Pg.112]

Zone-3 - Usually no danger of heart failure (ventricular fibrillation)... [Pg.680]

Hypertension /cardiac ischemia/vaso cons trie tion/central 4- blood pressure Hypertension/cardiac ischemia/skel. muscle blood flow Cardiac inotropy bronchospasm/heart rate/ventricular fibrillation Fascil. cardiac arrest/impairs cardiac perform... [Pg.171]

Kanashiro, M., Matsubara, T., Goto, T., and Sakamoto, N. (1993). Cyprid-ina luciferin analog reduces the incidence of ischemia/reperfusion-induced ventricular fibrillation. Jpn. J. Pharmacol. 63 47-52. [Pg.409]

Furthermore, under certain conditions (e.g. local unidirectional block) it is possible that the activation wavefront is delayed and encounters areas already repolarized. This may result in a circulating wave-front (= reentrant circuit reentrant arrhythmia), from which centrifugal activation waves originate and elicit life-threatening ventricular fibrillation. [Pg.97]

Ventricular fibrillation should be terminated by electrical defibrillation. Alternatively, lidocaine can be injected intravenously. In cases with lower frequency, ventricular tachyarrhythmia class I diugs such as aj marine, flecainide or propafenone are more effective as a result of the use-dependence of lidocaine. For prophylaxis treatment, amiodarone or sotalol may be helpful or the implantation of a cardioverter-defibrillator system. Acute amiodarone (i.v. in higher doses) can also terminate ventricular tachyarrhythmias. This action, however, seems to be mediated by its INa-blocking side effects and not (or less) by its class III like effects. [Pg.101]

Cardiac glycosides have a small ratio of toxic to therapeutic concentration. Possible adverse effects are nausea, vomiting, abdominal pain, diarrhoea, fatigue, headache, drowsiness, colour vision disturbances, sinus bradycardia, premature ventricular complexes, AV-block, bigeminy, atrial tachycardia with AV-Block, ventricular fibrillation. There are several mechanisms relevant for their toxic action (Table 2). [Pg.328]

Ventricular fibrillation Rapid disorganized contractions of the ventricles resulting in the inability of the heart to pump any blood to the body, which will result in death unless treated immediately... [Pg.368]

Proarrhytlimic effects (worsening of the existing arrhythmia or causation of a new arrhythmia) may occur, such as severe ventricular tachycardia or ventricular fibrillation. It is often difficult to distinguish proarrhytlimic effects from the patient s preexisting arrhythmia. [Pg.376]

Calcium is contraindicated in patients with hypercalcemia or ventricular fibrillation and in patients taking digitalis. Calcium is used cautiously in patients with cardiac disease. Hypercalcemia may occur when calcium is administered with the thiazide diuretics. When calcium is administered with atenolol there is a decrease in Hie effect of atenolol, possibly resulting in decreased beta blockade. There is an increased risk of digitalis toxicity when digitalis preparations are administered with calcium. The clinical effect of verapamil may be decreased when the drug is administered with calcium. Concurrent ingestion of spinach or cereal may decrease file absorption of calcium supplements. [Pg.641]

M (7/12 ventricular fibrillation after epinephrine challenge, 1/12 cardiac arrest)... [Pg.28]

Figure 4.2 Epicardial ECG recorded from an isolated blood-perfused rat heart at the moment of reperfusion. The heart was made regionally ischaemic by occluding a snare around the left anterior descending coronary artery and, after 10 min, reperfused by releasing the snare. Note the rapid onset of ventricular tachycardia (VT) and its subsequent degeneration into ventricular fibrillation (VF). Reproduced with permission from Lawson (1993). Figure 4.2 Epicardial ECG recorded from an isolated blood-perfused rat heart at the moment of reperfusion. The heart was made regionally ischaemic by occluding a snare around the left anterior descending coronary artery and, after 10 min, reperfused by releasing the snare. Note the rapid onset of ventricular tachycardia (VT) and its subsequent degeneration into ventricular fibrillation (VF). Reproduced with permission from Lawson (1993).
Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm... [Pg.2]

Treat polymorphic ventricular tachycardia (irregular rate and form) as ventricular fibrillation (see Table 1.9)... [Pg.10]


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Fibrillation, ventricular caused

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Idiopathic ventricular fibrillation (IVF

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Ventricular

Ventricular arrhythmias fibrillation

Ventricular fibrillation antiarrhythmics

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Ventricular fibrillation case studies

Ventricular fibrillation causes

Ventricular fibrillation clinical presentation

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Ventricular fibrillation diagnosis

Ventricular fibrillation epinephrine

Ventricular fibrillation etiology

Ventricular fibrillation incidence

Ventricular fibrillation lidocaine

Ventricular fibrillation magnesium

Ventricular fibrillation pacemaker

Ventricular fibrillation prevention

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