Automaticity, abnormal

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. 

The mechanism of abnormal impulse conduction is traditionally referred to as reentry. Reentry is often initiated as a result of an abnormal premature electrical impulse (abnormal automaticity) therefore, in these situations, the mechanism of the arrhythmia is both abnormal impulse formation (automaticity) and abnormal impulse conduction (reentry). In order for reentry to occur, three conditions must be present. There must be (1) at least two pathways down which an electrical impulse may... 

Premature ventricular complexes (PVCs) are common ventricular rhythm disturbances that occur in patients with or without heart disease and may be elicited experimentally by abnormal automaticity, triggered activity, or reentrant mechanisms. 

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. 

The antiarrhythmic drugs in class I suppress both normal Purkinje fiber and His bundle automaticity in addition to abnormal automaticity resulting from myocardial damage. Suppression of abnormal automaticity permits the sinoatrial node again to assume the role of the dominant pacemaker. 

Antiarrhythmic drugs are classified in four main groups based on their predominant mechanism of action. Antiarrhythmic agents in which class suppress abnormal automaticity and permit the sinoatrial node to again assume the role of the dominant pacemaker ... 

It blocks inactivated sodium channels. It also decreases calcium current and transient outward, delayed rectifier and inward rectifier potassium currents. It is a potent inhibitor of abnormal automaticity. It prolongs duration of action potential, refracto-... 

Calcium ion facilitates the toxic actions of cardiac glycosides by accelerating the overloading of intracellular calcium stores that appears to be responsible for digitalis-induced abnormal automaticity. Hypercalcemia therefore increases the risk of a digitalis-induced arrhythmia. The effects of magnesium ion appear to be opposite to those of calcium. These interactions mandate careful evaluation of serum electrolytes in patients with digitalis-induced arrhythmias. 

The acute phase of ischemia is followed by 3-6 h of predominantly sinus rhythm. Thereafter, the number of ventricular ectopic beats increases. In the subacute phase of infarction (12-24 h) ventricular arrhythmias often occur. One of the mechanisms involved is reinfarction. If there is no acute reinfarction involved, these arrhythmias have been suggested to originate from surviving strands of Purkinje fibers in the subendocardium. The predominant mechanism has been postulated to be abnormal automaticity in these fibers. These fibers exhibit an increased sensitivity for catecholamines. In some cases a combination of focal activity and reentry in these fibers may be possible. 

Class I antiarrthymic drugs block sodium channels and have varying effects on action potential duration (APD) and end resting potential (ERP). Quinidine and procainamide are the prototypic drugs in this class. These drugs act to (1) slow conduction velocity (phase 0), particularly in chronically depolarized cells, and (2) decrease abnormal automaticity (phase 4) in ectopic foci, and (3) may also decrease... 

Most arrhythmias arise either from aberrations in impulse generation (abnormal automaticity) or from a defect in impulse conduction. 

Actions Lidocaine, a local anesthetic, shortens phase 3 repoiarization and decreases the duration of the action potential (Figure 17.8). Unlike quinidine, which suppresses arrhythmias caused by increased normal automaticity, lidocaine suppresses arrhythmias caused by abnormal automaticity. Lidocaine, like quinidine, abolishes ventricular reentry. 

In a theoretical sense, drugs may have antiarrhythmic activity by directly altering conduction in several ways. First, a drug may depress the automatic properties of abnormal pacemaker cells. An agent may do this by decreasing the slope of phase 4 depolarization and/or by elevating threshold potential. If the rate of spontaneous impulse generation of the abnormally automatic foci becomes less than that of... 

Direct inhibition of Na/K-ATPase - T intracellular sodium J. APD and ERP, f Abnormal automaticity (possible arrhythmias) L Conduction velocity, reinforced by cholinomimetic action l APD and ERP, less significant than atrial actions... 

Sympathomimetic ( Jj-like) positive chronotropy, dromotropy, and inotropy t SA rate T Conduction velocity. 1 RP (possible AV nodal tachycardia) T Conduction velocity, T Phase 4 slope, T Abnormal automaticity... 

Nuss HB, Kaab S, Kass DA, Tomaselli GF, Marban E. Cellular basis of ventricular arrhythmias and abnormal automaticity in heart failure. Am J Physiol 1999 277(1 Pt 2) H80-91. 

Enhanced automaticity may occur in cells that normally display spontaneous diastolic depolarization— the sinus andAVnodes and the His-Purkinje system. [) Adrenergic stimulation, hypokalemia, and mechanical stretch of cardiac muscle cells increase phase 4 slope and so accelerate pacemaker rate, whereas acetylcholine reduces pacemaker rate both by decreasing phase 4 slope and by hyperpolarization (making the maximum diastolic potential more negative). In addition, automatic behavior may occur in sites that ordinarily lack spontaneous pacemaker activity e.g., depolarization of ventricular cells by ischemia) may produce such abnormal" automaticity. 

Abnormal automaticity Pacemaker activity that originates anywhere other than in the sinoatrial node... 

Ventricular tachycardia A very common arrhythmia, associated often with myocardial infarction ventricular tachycardia may involve abnormal automaticity or abnormal conduction, usually impairs cardiac output, and may deteriorate into ventricular fibrillation for these reasons it requires prompt management... 

Roden DM, Hoffman BF (Jun 1985). Action potential prolongation and induction of abnormal automaticity by low quinidine concentrations in canine Purkinje fibers. Relationship to potassium and cycle length. Circ Res 56(6) 857-867. 

Although fatal and poorly tolerated ventricular tachyarrhythmias are initiated and perpetuated by one of three fundamental mechanisms (reentry, triggered automaticity, and abnormal automaticity), clinically, they arise from a broad range of pathologic conditions that are difficult, if not impossible, to quantify. 

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