Premature ventricular contractions causes

Flecainide is very effective in suppressing premature ventricular contractions. However, it may cause severe exacerbation of arrhythmia even when normal doses are administered to patients with preexisting ventricular tachyarrhythmias and those with a previous myocardial... 

Flecainide is very effective in suppressing premature ventricular contractions. However, it may cause severe exacerbation of arrhythmia even when normal doses are administered to patients with preexisting ventricular tachyarrhythmias and those with a previous myocardial infarction and ventricular ectopy (see The Cardiac Arrhythmia Suppression Trial). The drug is well absorbed and has a half-life of approximately 20 hours. Elimination is both by hepatic metabolism and by the kidney. The usual dosage of flecainide is 100-200 mg twice a day. 

In addition to sinus tachycardia and tremor, vomiting is common after overdose. Hypotension, tachycardia, hypokalemia, and hyperglycemia may occur, probably due to -adrenergic activation. The cause of this activation is not fully understood, but the effects can be ameliorated by the use of B-blockers (see below). Cardiac arrhythmias include atrial tachycardias, premature ventricular contractions, and ventricular tachycardia. In severe poisoning (eg, acute overdose with serum level > 100 mg/L), seizures often occur and are usually resistant to common anticonvulsants. Toxicity may be delayed in onset for many hours after ingestion of sustained-release tablet formulations. 

TheophyUine decreases peripheral resistance, increases cardiac output, and causes a central vagal effect. Palpitations, sinus bradycardia, extrasystoles, hypotension, ventricular tachycardia, premature ventricular contractions (PVCs), and cardiac arrest have been reported. Although cardiovascular effects are generaUy mUd and transient, serious reactions, such as ventricular arrhythmias, can develop without warning. Patients should be carefuUy monitored. 

A. Amantadine intoxication causes agitation, visual hallucinations, nightmares, disorientation, delirium, slurred speech, ataxia, myoclonus, tremor, and sometimes seizures. Anticholinergic manifestations include dry mouth, urinary retention, and mydriasis. Rarely, ventricular arrhythmias including torsade de pointes (see p 14) and multifocal premature ventricular contractions may occur. Amantadine has also been reported to cause heart failure. 

Arrhythmias arise from ectopic foci in the cardiac tissue. Recall that all cardiac myocytes have the potential for spontaneous depolarization because of their smooth muscle-like properties and the close proximity of the cell membrane to depolarization threshold. Normally, these foci are eliminated by the powerful depolarization of the SA nodal cells. Unopposed, these foci generate depolarizations that cause small premature contractions and inhibit full contraction of cardiac muscle in response to the normal SA nodal depolarization. This is of primary importance in ventricular tissue. 

Ventricular arrhythmias arise most often from cells in the bundle of His and Purkinje s fibers. These ectopic foci can cause premature contraction of ventricular cells, resulting in no beneficial... 

All cardiac glycosides preparations have the potential to cause toxicity. Because the minimal toxic dose of the glycosides is only two- to threefold the therapeutic dose, intoxication is quite common. In mild to moderate toxicity, the common symptoms are anorexia, nausea and vomiting, muscular weakness, bradycardia, and ventricular premature contractions. The nausea is a result of excitation of the chemoreceptor trigger zone in the medulla. In severe toxicity, the common symptoms are blurred vision, disorientation, diarrhea, ventricular tachycardia, and AV block, which may progress into ventricular fibrillation. It generally is accepted that the toxicity of the cardiac glycosides results from inhibition of the Na /K -ATPase pump, which results in increased intracellular levels of Ca ". Hypokalemia (decreased potassium), which can be induced by coadministration of... 

---