Ventricular tachycardia chronic recurrent

Ventricular tachycardia (VT) is defined by three or more repetitive PVCs occurring at a rate greater than 100 beats/min. It occurs most commonly in acute myocardial infarction (MI) other causes are severe electrolyte abnormalities (e.g., hypokalemia), hypoxemia, and digitalis toxicity. The chronic recurrent form is almost always associated with underlying organic heart disease (e.g., idiopathic dilated cardiomyopathy or remote MI with left ventricular [LV] aneurysm). 

FIGURE 6-2. Algorithm for the treatment of acute (top portion) paroxysmal supraventricular tachycardia and chronic prevention of recurrences (bottom portion). Note For empiric bridge therapy prior to radiofrequency ablation procedures, calcium channel blockers (or other atrioventricular [AV] nodal blockers) should not be used if the patient has AV reentry with an accessory pathway. (AAD, antiarrhythmic drugs AF, atrial fibrillation AP, accessory pathway AVN, atrioventricular nodal AVNRT, atrioventricular nodal reentrant tachycardia AVRT, atrioventricular reentrant tachycardia DCC, direct-current cardioversion ECG, electrocardiographic monitoring EPS, electrophysiologic studies PRN, as needed VT, ventricular tachycardia.)... 

Maloney JD, Nissen RG, McColgan JM. Open clinical studies at a referral center chronic maintenance tocainide therapy in patients with recurrent sustained ventricular tachycardia refractory to conventional antiarrhythmic agents. Am Heart J 1980 100(6 Pt 2) 1023-30. 

Cardiovascular Recurrent ventricular tachycardia has been attributed to chronic exposure to aluminium in a 20-year-old man [2" ]. 

Arrhythmias, including prevention of recurrent paroxysmal supraventricular tachycardia and control of ventricular resting rate in chronic atrial fibrillation or flutter (with di-goxin) PO 240-480 mg/day in 3-4 divided doses. 

Cardiovascular effects include tachycardia, hypertension, and increased cardiac irritability large intravenous doses can cause cardiac failure. Cardiac dysrhythmias have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines (17), along with slowed cardiac conduction secondary to local anesthetic effects. Myocardial infarction has increased as a complication of cocaine abuse (7,8). Dilated cardiomyopathies, with subsequent recurrent myocardial infarction, have been associated with long-term use of cocaine, raising the possibility of chronic effects on the heart (18). Many victims have evidence of pre-existing fixed coronary artery disease precipitated by cocaine (SEDA-9, 35) (19-21). However, myocardial infarction has been noted even in young intranasal users with no evidence of coronary disease (22), defined by autopsy or angiography (23,24). If applied to mucous membranes, cocaine causes local vasoconstriction, and, with chronic use, necrosis. 

Verapamil (80 mg p.o. q. 6 to 8 hours) is indicated in the management of Prinzmetal s or variant angina or unstable or chronic, stable angina pectoris verapamil (0.075 to 0.15 mg/kg rv pnsh over a 2-minnte period) is indicated in the treatment of supraventricnlar tachyarrhythmias verapamil (240 to 480 mg p.o. daily) is indicated in the prevention of recurrent paroxysmal supraventricular tachycardia verapamil (240 to 320 mg p.o. daily) is indicated in the control of the ventricular rate in digitalized patients with chronic atrial flatter and/or fibrillation and verapamil (80 mg p.o. t.i.d.) is indicated in the management of hypertension. 

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