Ventricular tachyarrhythmias

Implantable tachyrhythmia devices, available for some years, address far less dangerous atrial tachyarrhythmias and fibrillation. The technical barriers to counteracting ventricular tachyarrhythmias and fibrillation using massive shocks have been formidable and are compounded by the possibiUty of causing the very problem the shock is designed to overcome. Newer tachyrhythmia devices are being readied that can safely regulate arrhythmias across the hiU spectmm. 

Ventricular fibrillation should be terminated by electrical defibrillation. Alternatively, lidocaine can be injected intravenously. In cases with lower frequency, ventricular tachyarrhythmia class I diugs such as aj marine, flecainide or propafenone are more effective as a result of the use-dependence of lidocaine. For prophylaxis treatment, amiodarone or sotalol may be helpful or the implantation of a cardioverter-defibrillator system. Acute amiodarone (i.v. in higher doses) can also terminate ventricular tachyarrhythmias. This action, however, seems to be mediated by its INa-blocking side effects and not (or less) by its class III like effects. 

First, drug-induced lengthening of the QT interval has been associated with the occurrence of ventricular tachyarrhythmias, namely TdP, a polymorphous ventricular arrhythmia that may cause syncope and degenerate into ventricular fibrillation and sudden death although the incidence of TdP is a rare event (usually, less than 1 in 100 000) [32], even a low risk is not justified for drugs with uncertain benefits or drugs providing only symptomatic improvement of a mild disease. 

Another unanswered question is the evaluation of the effect on cardiac repolarization of oncologic drugs, for which the thorough QT/QTc study in volunteers cannot be performed [166], In these cases, not only central tendency (i.e. mean QTc increase) and proportion of outliers but also other findings such as syncope, ventricular tachyarrhythmias and other cardiac effects should be more closely defined. 

Arrhythmias can range from isolated PVC s, coupled beats, non-sustained ventricular tachyarrhythmias (NSVT), sustained ventricular tachyarrhythmias (SVT) and, ultimately, ventricular fibrillation (VF). It is generally... 

This group consists of j3-adrenergic receptor blockers, the antiarrhythmic activity of which is associated with inhibition of adrenergic innervation action of the circulatory adrenaline on the heart. Because all 8-adrenoblockers reduce stimulatory sympathetic nerve impulses of catecholamines on the heart, reduce transmembrane sodium ion transport, and reduce the speed of conduction of excitation, sinoatrial node and contractibility of the myocardium is reduced, and automatism of sinus nodes is suppressed and atrial and ventricular tachyarrhythmia is inhibited. 

QRS complex, ventricular tachyarrhythmias, frequent ventricular ectopic beats, or tachycardia) dictates immediate discontinuation of quinidine closely monitor the ECG. 

Abstract Two thirds of the nearly half a million deaths per year in the United States due to sudden cardiac death (SCD) is attributed to coronary artery disease (CAD) and most commonly results from untreated ventricular tachyarrhythmias. Patients with ischemic cardiomyopathy and left ventricular dysfunction are at highest risk for SCD, but this still defines only a small subset of patients who will suffer SCD. Multiple lines of evidence now support the superiority of implantable cardioverter defibrillator (ICD) therapy over antiarrhythmic therapy for both primary and secondary prevention of SCD in advanced ischemic heart disease. Optimization of ICD therapy in advanced ischemic cardiomyopathy includes preventing right ventricular pacing as well as the use of highly effective anti-tachycardia pacing to reduce the number of shocks. While expensive, ICD therapy has been shown to compare favorably to the accepted standard of hemodialysis in cost effectiveness analyses. 

Sudden cardiac death (SCD) is defined as a sudden, unexpected death from a cardiac cause less than an hour after the onset of cardiac symptoms. SCD most commonly results from cardiac arrest due to lethal ventricular tachyarrhythmias. SCD usually... 

Implantable cardioverter defibrillators, on the other hand, have demonstrated a remarkable effectiveness in prevention of SCD, with an overall 1-year survival rate of 92% in patients with documented life-threatening ventricular tachyarrhythmias [26]. Three randomized, controlled trials have demonstrated the ICD to be superior to antiarrhythmic medications in the secondary prevention of SCD [27-29]. Recent primary prevention studies have also demonstrated improved... 

Fromer M, Brachmann J, Block M, et al. Efficacy of automatic multimodal device thempy for ventricular tachyarrhythmias as delivered by a new implantable pacing cardioverter-defibrillator. Results of a European multicenter study of 102 implants. Circulation. Aug 1992 86(2) 363-374. 

Higgins SL, Hummel JD, Niazi IK, et al. Cardiac resynchronization therapy for the treatment of heart failure in patients with intraventricular conduction delay and malignant ventricular tachyarrhythmias, [see comment]. J. Am. Coll. Cardiol. 2003 42 1454-9. 

Blockers are antiarrhythmics of class II according to the Vaughan-Williams classification, effective in the treatment of both supraventricular and ventricular tachyarrhythmias. These drugs can also reduce ectopic beats, especially if they are a result of sympathetic activity. Sotalol is a racemic mixture of the -blocking L-isomer and the class III antiarrhythmic D-isomer. This racemic mixture as well as D-sotalol are used as class Ill-antiarrhythmic. 

Class Ill-agents, used clinically, are rare, with amiodarone as the best-known example. Several experimental preparations are the subject of clinical investigation. Amiodarone has shown to be effective in the treatment of various ventricular tachyarrhythmias and one of its major advantages is... 

Class la Supraventricular tachyarrhythmias Certan ventricular tachyarrhythmias... 

ClassIb Ventricular tachyarrhythmias (in particular during the management of acute myocardial infarction hdocaine)... 

II.b.2.1. Prokinetic agents. Cisapride cisapride treatment can be demonstrated to improve sphincter and motor function and to improve modestly the symptoms of heartburn. However, it is relatively ineffective in severe disease, and adverse effects of impaired intracardiac electrical conduction causing ventricular tachyarrhythmias have resulted in its withdrawal from general use. 

The cardiac toxicity of quinidine includes A-V and intraventricular block, ventricular tachyarrhythmias, and depression of myocardial contractility. Ventricular arrhythmia induced by quinidine leading to a loss of consciousness has been referred to as quinidine syncope. This devastating side effect is more common in women than in men and may occur at therapeutic or subtherapeutic plasma concentrations. 

Acute cardiovascular reactions to procainamide administration include hypotension, A-V block, intraventricular block, ventricular tachyarrhythmias, and complete heart block. The drug dosage must be reduced or even stopped if severe depression of conduction (severe prolongation of the QRS interval) or repolarization (severe prolongation of the QT interval) occurs. 

The major toxic reactions to disopyramide administration include hypotension, congestive heart failure, and conduction disturbances. These effects are the result of disopyramide s ability to depress myocardial contractility and myocardial conduction. Although disopyramide initially may produce ventricular tachyarrhythmias or ventricular fibrillation in some patients, the incidence of disopyramide-induced syncope in long-term therapy is not known. Most other toxic reactions (e.g., dry mouth, blurred vision, constipation) can be attributed to the anticholinergic properties of the drug. 

As with other members of class IB, mexiletine slows the maximal rate of depolarization of the cardiac membrane action potential and exerts a negligible effect on repolarization. Mexiletine demonstrates a rate-dependent blocking action on the sodium channel, with rapid onset and recovery kinetics suggesting that it may be more useful for the control of rapid as opposed to slow ventricular tachyarrhythmias. 

The most profound effect of adenosine is the induction of an A-V block within 10 to 20 seconds of administration. Mild sinus slowing may be observed initially followed by sinus tachycardia. There is no effect on the QRS duration or QT interval. Rarely, an adenosine bolus injection is accompanied by atrial fibrillation or ventricular tachyarrhythmias. 

Magnesium sulfate may be effective in terminating refractory ventricular tachyarrhythmias, particularly polymorphic ventricular tachycardia. DigitaUs-induced arrhythmias are more likely in the presence of magnesium deficiency. Magnesium sulfate can be administered orally, intramuscularly, or, preferably, intravenously,... 

Contraindications are atrial or ventricular tachyarrhythmias, hyperthyroidism and pheochromocytoma. 

Adverse effects include SA block or arrest, high grade AV block, ventricular tachycardia, arrhythmia or ventricular asystole, polymorphic ventricular tachyarrhythmia, hypotension (particularly when given IV), cinchonism, tinnitus, loss of hearing, gastrointestinal upset, severe headache, diplopia, photophobia, etc. 

It is indicated in prophylaxis or treatment of ventricular arrhythmias associated with Ml, digitalis intoxication, ventricular tachyarrhythmia, in patients predisposed to ventricular arrhythmias during general anaesthesia. 

These are class IC drugs with similar pharmacological profiles and with the same indication range and adverse effects. They are mainly used for the treatment of severe, lifethreatening ventricular tachyarrhythmias, and non-sustained ventricular tachycardia or high-frequency premature ventricular beats. The main adverse effects are cardiovascular, including proarrhythmic actions and severe negative inotropic effects, especially in patients with impaired cardiac function. Both flecainide and encainide increase the risk of sudden death in patients with myocardial infarction and asymptomatic unsustained ventricular arrhythmias. 

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. 

Betsuyaku T, Nnebe N, Sundset R, et al. 2006. Overexpression of cardiac connexin 45 increases susceptibility to ventricular tachyarrhythmias in vivo. Am J Physiol Heart Circ Physiol 290 H163-H171. 

Therapeutic uses Quinidine is used in the treatment of a wide variety of arrhythmias, including atrial, AV junctional, and ventricular tachyarrhythmias. Quinidine is used to maintain sinus rhythm after direct current cardioversion of atrial flutter or fibrillation and to prevent frequent ventricular tachycardia. 

These are Class IB drugs with actions similar to those of lidocaine. These agents can be administered orally. Mexiletine [mex IL e teen] is used for chronic treatment of ventricular arrhythmias associated with previous myocardial infarction. Tocainide [toe KAY nide] is used for treatment of ventricular tachyarrhythmias. Tocainide has pulmonary toxicity, which may lead to pulmonary fibrosis. 

Therapeutic uses Amiodarone is effective in the treatment of severe refractory supraventricular and ventricular tachyarrhythmia. Its clinical usefulness is limited by its toxicity. 

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