Automatic atrial tachycardia

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

Common supraventricular tachycardias requiring drug treatment are atrial fibrillation (AF) or atrial flutter, paroxysmal supraventricular tachycardia (PSVT), and automatic atrial tachycardias. Other common supraventricular arrhythmias that usually do not require drug therapy are not discussed in this chapter (e.g., premature atrial complexes, wandering atrial pacemaker, sinus arrhythmia, sinus tachycardia). 

Automatic atrial tachycardias such as multifocal atrial tachycardia appear to arise from supraventricular foci with enhanced automatic properties. Severe pulmonary disease is the underlying precipitating disorder in 60% to 80% of patients. 

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-... 

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. 

Type II drugs include /Tadrenergic antagonists clinically relevant mechanisms result from their antiadrenergic actions. /3- Blockers are most useful in tachycardias in which nodal tissues are abnormally automatic or are a portion of a reentrant loop. These agents are also helpful in slowing ventricular response in atrial tachycardias (e.g., AF) by their effects on the AV node. 

Esmolol Atrial fibrillation and flutter, automatic tachycardias... 

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. 

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. 

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

Altered rate of automatic discharge or abnormality of the mechanism by which an impulse is generated from a centre in the nodes or conducting tissue, is one cause of cardiac arrhythmia, e.g. atrial fibrillation, flutter or tachycardia. 

Atrial tachycardia Enhanced automaticity, DAD-related automaticity, or reentry within the atrium Same as atrial fibrillation Same as atrial fibrillation Ablation of tachycardia focus ... 

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