Paroxysmal ventricular tachycardia

PCA Patient-controlled analgesia PVT Paroxysmal ventricular tachycardia... 

Oral Premature atrial, AV junctional and ventricular contractions paroxysmal atrial (supraventricular) tachycardia paroxysmal AV junctional rhythm atrial flutter paroxysmal and chronic atrial fibrillation established atrial fibrillation when therapy is appropriate paroxysmal ventricular tachycardia not associated with complete heart block maintenance therapy after electrical conversion of atrial fibrillation or flutter. Parenteral When oral therapy is not feasible or when rapid therapeutic effect is required. 

Ora/-Adverse reactions requiring discontinuation include Pulmonary infiltrates or fibrosis paroxysmal ventricular tachycardia CHF elevation of liver enzymes visual disturbances solar dermatitis blue discoloration of skin hyperthyroidism hypothyroidism. Adverse reactions occurring in at least 3% of patients include CFIF Gl complaints (nausea, vomiting, constipation, anorexia) dermatologic reactions (photosensitivity, solar dermatitis) neurologic problems (malaise, fatigue, tremor/abnormal involuntary movements, lack of coordination, abnormal gait/ataxia, dizziness, paresthesias) abnormal liver function tests. 

Maintenance of normal sinus rhythm after conversion of atrial fibrillation or flutter, prevention of premature atrial, AV, and ventricular contractions paroxysmal atrial tachycardia paroxysmal AV functional rhythm atrial fibrillation atrial flatter paroxysmal ventricular tachycardia not associated with complete heart block PO 100-600 mg q4-6h. (Long-acting) 324-972 mg q8-12h. IV 200-400 mg. 

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

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. 

Fauchier JP, Cosnay P, Neel C, Rouesnel P, Bonnet P, Quilhet L. Traitement des tachycardies supraventriculaires et ventriculaires paroxystiques par le bepridil. [Treatment of supraventricular and paroxysmal ventricular tachycardia with bepridil.] Arch Mai Coeur Vaiss 1985 78(4) 612-19. 

Pulseless electrical activity (PEA)—The absence of a detectable pulse and the presence of some type of electrical activity other than ventricular fibrillation (VF) or paroxysmal ventricular tachycardia (PVT). 

Tocainide is used in the treatment of ventricular arrhythmias including unifocal and multifocal ventricular premature contractions, coupled ventricular premature contractions, and paroxysmal ventricular tachycardia. 

Sparteine has an underlying nascent stimulatory action on the ventricle which may prove dangerous in clinical therapy. Jourdan and Froment (74) found that sparteine injected into a chloralized dog, whose vagal and sympathetic nerves were severed and the AV conduction disrupted by section of the bundle, would first cause simple stimulation, then extra systoles, then paroxysmal ventricular tachycardia, and, finally, ventricular fibrillation. 

Procainamide is a class I anti-arrhythmic agent with actions similar to those of quinidine. It depresses myocardial automaticity and excitability and increases the effective refractory period of the atrium. It finds its application towards the suppression of ventricular extrasystoles and paroxysmal ventricular tachycardia. It is also useful in the control and management ofatrialfibrillation and premature atrial contractions. 

The uses of the antiarrhythmic drug are given in the Summaiy Drug Table Antiarrhythmic Drug3. In general these drugp are used to prevent and treat cardiac arrhythmias, such as premature ventricular contractions (PVCs), ventricular tachycardia (VT), premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), atrial fibrillation, and atrial flutter. Some of the antiarrhythmic dru are used for other... 

FIGURE 6-10. Decision algorithm for termination of paroxysmal supraventricular tachycardia. HF, heart failure LVEF, left ventricular ejection fraction PSVT, paroxysmal supraventricular tachycardia. (Algorithm adapted with permission from Tisdale JE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE,... 

PST Paroxysmal supraventricular tachycardia S3 Third heart sound (ventricular gallop)... 

AF, atrial fibrillation HF, heart failure 10, intraosseous PSVT, paroxysmal supraventricular tachycardia VF, ventricular fibrillation VT, ventricular tachycardia. 

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.)... 

Cardiovascular manifestations include hypertension and cardiac arrhythmias (e.g., heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation, and digitalis-induced arrhythmias). In severe hypokalemia (serum concentration <2.5 mEq/L), ECG effects include ST-segment depression or flattening, T-wave inversion, and U-wave elevation. 

Qninidine exhibits all of the pharmacological properties of qninine, including antimalar-ial, fever-redncing, and other properties. Quinidine is used in varions forms of arrhythmia for preventing tachycardia and atrial fibrillation, and particularly for preventing ciliary fibrillation, paroxysmal snpraventricnlar tachycardia, extrasystole, and ventricular tachycardia. However, it is a toxic drug and is nsed relatively rarely. 

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. 

Ventricular proarrhythmic effects in patients with atrial fibrillation/flutter A review of the world literature revealed reports of 568 patients treated with oral flecainide for paroxysmal atrial fibrillation/flutter (PAF). Ventricular tachycardia was experienced in 0.4% of these patients. Of 19 patients in the literature with chronic atrial fibrillation (CAF), 10.5% experienced ventricular tachycardia (VT) or ventricular fibrillation (VF). Flecainide is not recommended for use in patients with CAF. Case reports of ventricular proarrhythmic effects in patients treated with flecainide for atrial... 

Unlabeled Uses Control of hemodynamicallystableventriculartachycardia, control of rapid ventricular rate due to accessory pathway conduction in preexcited atrial arrhythmias, conversion of atrial fibrillation to normal sinus rhythm, in cardiac arrest with persistent ventricular tachycardia or ventricular fibrillation, paroxysmal supraventricular tachycardia, polymorphic ventricular tachycardia or wide complex tachycardia of uncertain origin, prevention of postoperative atrial fibrillation... 

Maintenance dosage for CHF control of ventricular rate in patients with atrial fibrillation treatment and prevention of recurrent paroxysmal atrial tachycardia PO, IV... 

Temporary control of rapid ventricular rate in atrial flBrillation or flutter, rapid conversion of paroxysmal supraventricular tachycardia to normal sinus rhythm IV push Initially, 0.25 mg/kg actual body weight over 2 min. May repeat in 15 min at dose of 0.35 mg/kg actual body weight. Subsequent doses individualized. IV Infusion / fter initial bolus injection, may begin infusion at 5-10 mg/hr may increase by 5 mg/hr up to a maximum of 15 mg/hr. Infusion duration should not exceed 24 hr. 

Overdose may induce ventricular extrasystoles and short paroxysms of ventricular tachycardia, a sensation of fullness in the head, and tingling of the extremities. Should an excessive elevation of blood pressure occur, it may be immediately relieved by an a-adrenergic blocking agent, e.g., phentolamine. 

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. 

It is indicated in prevention of atrial arrhythmia, atrial fibrillation or flutter, paroxysmal supraventricular tachycardia, ventricular premature beats and ventricular tachycardia. 

It is a anticonvulsant drug and depresses the ventricular automaticity and accelerates the AV conduction. It also reduces the duration of action potential like quinidine. It also shortens the QT interval. It mainly blocks inactivated Na+ channels. It is used for the suppression of ectopic beats and for prophylaxis of recurrent paroxysmal tachycardia and also for the treatment of rapid supraventricular or ventricular tachycardia. 

It is indicated in tachyarrhythmias associated with WPW syndrome, atrial flutter and fibrillation, paroxysmal tachyarrhythmias not responding to other agents. Ventricular tachycardia and ventricular arrhythmia refractory to other treatment. 

Ventricular and supraventricular tachycardia (especially those due to re-entry phenomena), atrial fibrillation and flutter (can convert recent-onset fibrillation or flutter to sinus rhythm) Paroxysmal supraventricular tachycardia, atrial or ventricular premature beats, atrial fibrillation, or flutter (slows ventricular rate)... 

Paroxysmal supraventricular tachycardia, atrial fibrillation and flutter. Not of benefit in treatment of ventricular arrhythmias Miscellaneous... 

Digoxin Atrial fibrillation and flutter with rapid ventricular response Adenosineldiopathic and re-entrant paroxysmal supraventricular tachycardia WPW, Wolf-Parkinson-White. 

This agent also has some class lA and class II effects. It is effective for the treatment of ventricular and supraventricular tachycardias (AV nodal and accessory pathway re-entry, atrial flutter and fibrillation). Propafenone is useful in converting recent-onset atrial fibrillation or flutter to sinus rhythm, and for terminating paroxysmal supraventricular tachycardia. Its pro-ariythmic and myocardial depressant effects limit its use, especially in patients with poor ventricular function. 

Adenosine is a nucleoside that occurs naturally throughout the body. Its half-life in the blood is less than 10 seconds. Its mechanism of action involves activation of an inward rectifier K+ current and inhibition of calcium current. The results of these actions are marked hyperpolarization and suppression of calcium-dependent action potentials. When given as a bolus dose, adenosine directly inhibits atrioventricular nodal conduction and increases the atrioventricular nodal refractory period but has lesser effects on the sinoatrial node. Adenosine is currently the drug of choice for prompt conversion of paroxysmal supraventricular tachycardia to sinus rhythm because of its high efficacy (90-95%) and very short duration of action. It is usually given in a bolus dose of 6 mg followed, if necessary, by a dose of 12 mg. An uncommon variant of ventricular tachycardia is adenosine-sensitive. The drug is less effective in the presence of adenosine receptor blockers such as theophylline or caffeine, and its effects are potentiated by adenosine uptake inhibitors such as dipyridamole. 

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. 

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