Procainamide fibrillation

Procainamide is intended for treating paroxysmal atrial tachycardia, atrial fibrillation, prematnre ventricular contraction, and ventricnlar tachycardia. For qnickly reaching therapeutic concentrations, parentemal introdnction of procainamide is preferred over cynidine. Synonyms of this drng are amidoprocaine, cardiorythmine, novocainamide, pronestyl, and others. 

Atrial fibrillation/flutter- Procainamide has been used to convert atrial fibrillation/flutter to sinus rhythm. 

Digitalis intoxication Exercise caution in the use of procainamide in arrhythmias associated with digitalis intoxication. Procainamide can suppress digitalis-induced arrhythmias however, if there is concomitant marked disturbance of AV conduction, additional depression of conduction and ventricular asystole or fibrillation may result. Consider use of procainamide only if discontinuation of digitalis, and therapy with potassium, lidocaine, or phenytoin are ineffective. 

First-degree heart block Exercise caution if the patient exhibits or develops first-degree heart block while taking procainamide dosage reduction is advised. If the block persists despite dosage reduction, evaluate the continuation of procainamide on the basis of current benefit vs risk of increased heart block. Predigitalization for atrial flutter or fibrillation Cardiovert or digitalize patients with atrial flutter or fibrillation prior to procainamide administration to avoid enhancement... 

Procainamide is an effective antiarrhythmic agent when given in sufficient doses at relatively short (3-4 hours) dosage intervals. Procainamide is useful in the treatment of premature atrial contractions, paroxysmal atrial tachycardia, and atrial fibrillation of recent onset. Procainamide is only moderately effective in converting atrial flutter or chronic atrial fibrillation to sinus rhythm, although it has... 

The effects of disopyramide are very similar to those of procainamide and quinidine. Its cardiac antimuscarinic effects are even more marked than those of quinidine. Therefore, a drug that slows atrioventricular conduction should be administered with disopyramide when treating atrial flutter or fibrillation. 

Madrid AH, et al. Comparison of flecainide and procainamide in cardioversion of atrial fibrillation. Eur Heart J 1993 ... 

Stambler BS, Wood MA, Ellenbogen KA. Antiarrhythmic actions of intravenous ibutilide compared with procainamide during human atrial flutter and fibrillation electrophysiological determinants of enhanced conversion efficacy. Circulation 1997 96( 12) 4298-4306. 

Volgman AS, et al. Conversion efficacy and safety of intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation. J Am Coll Cardiol 1998 3 I (6) 1414 1419. 

An 86-year-old woman was given adenosine 12 mg intravenously for sustained supraventricular tachycardia, which terminated but was followed by atrial fibrillation and paroxysmal ventricular tachycardia (24). Cardioversion was unsuccessful, but normal sinus rhythm was obtained with procainamide. This followed an anteroseptal myocardial infarction. 

A 54-year-old woman who was given lidocaine, 200 mg intravenously, for ventricular fibriUation during cardiopulmonary bypass, had a tonic-clonic seizure (28). The seizure occurred immediately after the administration of hdocaine and was reheved by the intravenous administration of thiopental and midazolam. Her ventricular fibrillation responded to procainamide 1 g intravenously over 10 minutes. 

The adverse effects of intravenous procainamide (400 mg up to three times infused over 10 minutes) have been reported in 60 adults with atrial flutter or fibrillation in a comparison with ibutihde (2). The adverse effects were headache in 11%, hypotension in 11%, flushing in 3.1%, dizziness in 3.1%, and hypesthesia in 3.1%. The mean fall in systolic blood pressure was about 20 mmHg and occurred at 30-35 minutes after infusion the corresponding fall in diastolic blood pressure was 10 mmHg. However, in seven patients there was severe hypotension, with a fall in diastolic blood pressure of up to 67 mmHg in three cases withdrawal of the infusion was required and these patients were treated with intravenous fluids, dopamine, or both. In the severe cases the hypotension occurred during or immediately after the infusion of procainamide. 

A comparison between procainamide and propafenone in 62 patients, who had undergone coronary artery bypass grafting or valvular surgery within 3 weeks and developed sustained atrial fibrillation, showed that both drugs converted the dysrhythmia to sinus rhythm in up to 76% of cases, but that propafenone did it more quickly (3). Symptomatic arterial hypotension occurred more frequently with procainamide (nine of 33 patients) than with propafenone (two of 29 patients). Other adverse effects of procainamide were nausea (n = 2) and junctional escape rhythm (n = 2). 

Geelen P, O Hara GE, Roy N, Talajic M, Roy D, Plante S, Turgeon J. Comparison of propafenone versus procainamide for the acute treatment of atrial fibrillation after cardiac surgery. Am J Cardiol 1999 84(3) 345-7. 

Rea R F, Hamdan M, Schomer S J et al 1991 Inhibitory effects of procainamide on sympathetic nerve activity in humans. Circulation Research 69 501-508 Reef V 1999 Arrhythmias. In Marr C (ed) Cardiology of the horse. Saunders, London, pp. 179-209 Reef V B, Levitan C W, Spencer P A 1988 Factors affecting prognosis and conversion in equine atrial fibrillation. Journal of Veterinary Internal Medicine 2 1-6... 

The primary toxicities observed with procainamide are cardiovascular in nature. Initially, a tachycardia may occur due to procainamide s anticholinergic properties or as a reflex response to vasodilation. Cardiac conduction disturbances may occur. On the ECG, these may be displayed as prolongation of the QRS and/or QTc duration. Heart block, bradycardia, and asystole have been reported. Procainamide can also cause ventricular tachycardia, ventricular fibrillation, and Torsades de Pointes. Severe hypotension due to decreases in cardiac output and/or vasodilation may be seen. Altered mental status and seizure activity can occur in procainamide toxicity. 

Procainamide, proprietary name Pronestyl, is used for therapy of PVCs, ventricular tachycardia, atrial fibrillation, and paroxysmal atrial tachycardia. Its mechanism of action is similar to that of quinidine in that it increases the threshold membrane potential by blocking potassium outflow, reducing excitability and contraction velocity in Purkinje s fibers and ventricular muscle. 

Patients with Wolff-Parkinson-White (WPW) syndrome may have several different tachycardias that are treated acutely by different strategies orthodromic reentry (adenosine), antidromic reentry (adenosine or procainamide), and atrial fibrillation (procainamide or amiodarone). AV nodal blocking drugs are contraindicated with WPW syndrome and atrial fibrillation. 

Procainamide (e.g., Pronestyl) II If Premature atnal depolarization, atrial fibrillation, Wolff-Parkinson-White, ventricular tachycardia, atrial flutter, premature ventricular depolarization. Fewer Gl effects and weaker anticholinergic effects than quinidine, but similar cardiac toxicity. Lupus-like syndrome and other hypersensitivity reactions. 

MADIT was the first randomized trial to show that the ICD, used as a prophylactic, can reduce the risk of death in high-risk patients. The MADIT assessed patients who had coronary artery disease and a prior Q-wave myocardial infarction. To be included, patients had to have (a) asymptomatic nonsustained ventricular tachycardia recorded on a 24-h Hotter monitor, (b) a left ventricular ejection fraction of < 0.35 and, (c) inducible sustained monomorphic ventricular tachycardia or ventricular fibrillation not suppressed by procainamide at electrophysiology testing. 

Cardiovascular Intravenous procainamide had a prodysrhythmic effect when it was given as a single 1000 mg bolus during an electrophysiological study in a patient with myotonic dystrophy type 1 [SO J. During ventricular pacing, ventricular tachycardia and fibrillation occurred and required DC cardioversion. By slowing cardiac conduction, procainamide, as do other sodium channel blockers, worsens abnormalities already present in the hearts of patients with myotonic dystrophy t)q)e 1. 

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