Tachycardia automatic

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. 

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. 

Type IV drugs inhibit calcium entry into the cell, which slows conduction, prolongs refractoriness, and decreases SA and AV nodal automaticity. Calcium channel antagonists are effective for automatic or reentrant tachycardias that arise from or use the SA or AV nodes. 

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. 

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. 

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. 

Verapamil Calcium channel (ICa-i type) blockade Slows SA node automaticity and AV nodal conduction velocity decreases cardiac contractility t reduces blood pressure Supraventricular tachycardias Oral, IV hepatic metabolism caution in patients with hepatic dysfunction Toxicity Interactions See Chapter 12... 

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. 

Adenosine is a naturally occurring nucleoside, but at high doses the drug decreases conduction velocity, prolongs the refractory period, and decreases automaticity in the AV node. Intravenous adenosine is the drug of choice for abolishing acute supraventricular tachycardia. It has low toxicity, but causes flushing, chest pain and hypotension. Adenosine has an extremely short duration of action (about 15 seconds). 

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. 

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