Ventricular depolarization premature

Asymptomatic ventricular premature depolarizations should not be treated with antiarrhythmic drug therapy. 

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

Ventricular premature depolarizations (VPDs) are ectopic electrical impulses originating in ventricular tissue, resulting... 

Ventricular premature depolarizations occur with variable frequency, depending on underlying comorbid conditions. The prevalence of complex or frequent VPDs is approximately 33% and 12% in men with and without CAD, respectively 34 in women, the prevalence of complex or frequent VPDs is 26% and 12% in those with and without CAD, respectively.35 Ventricular premature depolarizations occur more commonly in patients with ischemic heart disease, a history of myocardial infarction, and HF due to LV dysfunction. They may also occur as a result of hypoxia, anemia, and following cardiac surgery. 

Ventricular premature depolarizations occur as a result of abnormal ventricular automaticity, as a result of enhanced activity of the sympathetic nervous system and altered electro-physiologic characteristics of the heart during myocardial ischemia and following myocardial infarction. 

Clinical Presentation and Diagnosis Ventricular Premature Depolarizations ... 

Avoid treatment of patients with asymptomatic ventricular premature depolarizations. Unlabeled uses ... 

It is indicated in ventricular arrhythmia, ventricular premature depolarization and paroxysmal ventricular tachycardia, supra-ventricular tachycardia and atrial arrhythmia. 

The arrhythmias mainly observed are ventricular tachycardias, ventricular premature depolarizations and accelerated idioventricular rhythms as well as atrioventricular dissociation. 

Cairns JA, Connolly SJ, Roberts R, et al. Randomized trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarizations CAMIAT. Lancet 1997 349 675-682. 

Arrhythmias Originating in the Ventricie Ventricular Premature Depolarization ... 

I. Pharmacology. The neuronal membrane-stabilizing actions of phenytoin make this a popular drug for sustained control of aoute and ohronic seizure disorders and a useful drug for certain cardiac arrhythmias. Because of the relatively slow onset of anticonvulsant action, phenytoin is usually administered after diazepam. At serum concentrations considered therapeutic for seizure control, phenytoin acts similarly to lidocaine to reduce ventricular premature depolarization and suppress ventricular tachycardia. After intravenous administration, peak therapeutic effects are attained within 1 hour. The therapeutic serum concentration for seizure control is 10-20 mg/L. Elimination is nonlinear, with an apparent half-life averaging 22 hours. Fosphenytoin, a prodrug of phenytoin for intravenous use, is converted to phenytoin after injection, with a conversion half-life of 8-32 minutes. 

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