Ectopic atrial tachycardia

Verapamil is useful for slowing the ventricular response to atrial tachyarrhythmias, such as atrial flutter and fibrillation. Verapamil is also effective in arrhythmias supported by enhanced automaticity, such as ectopic atrial tachycardia and idiopathic left ventricular tachycardia. 

Automatic atrial tachycardias such as multifocal atrial tachycardia appear to arise from supraventricular foci that have enhanced automatic properties. It is presumed that multifocal atrial tachycardia is the result of multiple ectopic atrial pacemakers, which account for the variable and differing P-wave morphology. In unifocal atrial tachycardia (sometimes referred to as ectopic atrial tachycardia), a single P-wave morphology different from that of sinus rhythm is recorded. In either case, the underlying, precipitating disorder present in the major-... 

The most commonly reported cardiac signs of toxicity are dysrhythmias, such as ventricular ectopic depolarization, second- and third-degree heart block, junctional tachycardia, atrial tachycardia with block, ventricular tachycardia, sinoatrial block, and sinus arrest. 

Amiodarone is indicated for the suppression and prevention of documented life-threatening, recurrent, ventricular tachycardia or fibrillation when other agents have failed. Amiodarone is also used in the management of supraventricular tachyarrhythmias including paroxysmal atrial fibrillation and atrial flutter, ectopic or multifocal atrial tachycardia, junctional tachycardia, and paroxysmal reentrant supraventricular tachycardia when other agents have failed to suppress or prevent their recurrence. Amiodarone has also been used to treat wide-complex tachycardia of uncertain mechanism. 

Other supraventricular arrhythmias, such as supraventricular paroxysmal tachycardia or atrial tachycardia secondary to an ectopic focus, are much less frequent. 

Paroxysmal atrial tachycardia occurs with a sudden onset of 140-220 beats/minute, which may cease abruptly. The focus is ectopic—it can be anywhere in the atrium. 

Quinidine (e.g., Cin-Quin) Depresses automaticity of ectopic foci. Siows conduction veiocity in atria His-Purkinje ceils. Prolongs refractory period throughout heart (except nodes) and accessory pathways. Has anticholinergic effects which may actuaiiy enhance A-V conduction in patients with rapid atrial depolarization. Multifocal atrial tachycardia, premature atrial depolarization, premature ventricular depolarization, atrial fibrillation (these result from increased automaticity of ectopic foci), and ventricular tachycardia. Torsades de pointes (recurrent, temporary arrhythmia), increases ventricle response to atrial tachyarrhythmia, nausea, vomiting, diarrhea, hypersensitivity, cinchonism, thrombocytopenic purpura. 

Atrial tachycardia (AT) is a rapid ectopic rhythm originating in one of the atria. The onset tends to be sudden. Its rate is usually found between about 130-240 b.p.m., and the rhythm may conduct in a 1 1 fashion to the ventricles. Thus, the rapidly conducted varieties may likely enter the detection zone(s) of the ICD. The atrial electrogram (AEGM) P wave morphology for a dual chamber ICD may show a noticeable change with the onset tachycardia, while the VEGM should remain the same absent BBA. 

The indications for use of disopyramide are similar to those for quinidine, except that it is not approved for use in the prophylaxis of atrial flutter or atrial hbrUla-tion after DC conversion. The indications are as follows unifocal premature (ectopic) ventricular contractions, premature (ectopic) ventricular contractions of multifocal origin, paired premature ventricular contractions (couplets), and episodes of ventricular tachycardia. Persistent ventricular tachycardia is usually treated with DC conversion. 

Amiodarone is effective in maintaining sinus rhythm in most patients with paroxysmal atrial hbrillation and in many patients with persistent atrial hbrillation. It is also effective in preventing recurrences of A-V nodal reentry and atrial tachyarrhythmias and in the prevention of reentrant rhythms and atrial hbrillation in patients with Wohf-Parkinson-White syndrome. Also, it is the most efficacious therapy for postoperative junctional ectopic tachycardia. 

The antiarrhythmic action is due to cardiac adrenergic blockade. It decreases the slope of phase 4 depolarization and automaticity in SA node, Purkinje fibres and other ectopic foci. It also prolongs the effective refractory period of AV node and impedes AV conduction. ECG shows prolonged PR interval. It is useful in sinus tachycardia, atrial and nodal extrasystoles. It is also useful in sympathetically mediated arrhythmias in pheochromocytoma and halothane anaesthesia. 

As with most data for reboxetine, this information primarily comes from summary papers rather than primary sources (473, 474). With this caveat, the adverse-effect profile of reboxetine is consistent with its pharmacology as an NSRI. Thus, it is similar to that of desipramine and maprotiline but without the risk of serious CNS (i.e., seizures, delirium) or cardiac (i.e., conduction disturbances) toxicity. The most common adverse effects of reboxetine are dry mouth, constipation, urinary hesitancy, increased sweating, insomnia, tachycardia, and vertigo. Whereas the first three adverse effects are commonly called anticholinergic, they are well known to occur with sympathomimetic drugs as well. In other words, these effects can be either the result of decreased cholinergic tone or increased sympathetic tone, although they tend to be more severe with the former than the latter. In contrast to TCAs, reboxetine does not directly interfere with intracardiac conduction. The tachycardia produced by reboxetine, however, can be associated with occasional atrial or ventricular ectopic beats in elderly patients. 

Class I drugs have a local anaesthetic-like action, blocking the inward current in sodium channels. This depresses the fast depolarisation (phase 0) which initiates each action potential (Figure 8.5). This membrane-stabilising effect makes them valuable for the treatment of ectopic and tachycardic arrhythmias, such as atrial and ventricular fibrillation, extrasystoles, supraventricular and ventricular tachycardia. Class I drugs also decrease contractility. A sub-classification is made according to the effects on... 

Digoxin (see p. 158) shortens the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in Purkinje fibers. Digoxin is used to control the ventricular response rate in atrial fibrillation and flutter. At toxic concentrations, digoxin causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation. [Note This arrhythmia is usually treated with lidocaine or phenytoin.]... 

This occurs in otherwise healthy individuals, who possess an anomalous (accessory) atrioventricular pathway they often experience attacks of paroxj mal AV re-entrant tachycardia or atrial fibrillation. Drugs that both suppress the initiating ectopic beats and delay conduction through the accessory pathway are used to prevent attacks e.g. flecainide, sotalol or amiodarone. Verapamil and digoxin may increase conduction through the anomalous pathway and should not be used. Electrical conversion may be needed to restore sinus rhythm when the ventricular rate is very rapid. Radiofrequency ablation of aberrant pathways will almost certainly provide a cure. 

P-ARK An enzyme that phosphoylates the occupied form of a G-protein coupled receptor, e.g. the 6-adrenoceptor, leading to uncoupling of that receptor and desensitization. ARMI age-related memory impairment, arrhythmia (dysrhythmia) An abnormality of heart rhythm or rate of heartbeat, usually caused by disturbance of the electrical impulses and their conduction within the heart. They include ectopic beats (isolated irregular beats), tachycardias (too fast a heartbeat), bradycardias (too slow a heartbeat) and atrial flutter and ventricular fibrillation. Arthus reaction A severe local inflammatory response, a skin reaction characterized by erythema, oedema, necrosis, local haemorrhage. A type III hypersensitivity reaction. Arunlakshana and Schild plot See Schild plot, ascites fluid The fluid that accumulates in the peritoneal cavity during certain pathological conditions, aspiration The withdrawal of fluid or tissue from the body by suction. 

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