Ectopic foci

Enhanced automaticity occurs in hypoxia, hypokalemia, hypercarbia, excessive sympathetic nervous system stimulation, or high concentrations of catecholamines. These conditions may lead to arrhythmias. Decreased automaticity may also lead to production of arrhythmias by enhancing ectopic activity in latent pacemakers (ectopic foci) or by altering conductivity and refractoriness in conduction pathways of myocardium. 

Glass lA Antiarrhythmic Agents. Class lA antiarrhythmic agents decrease automaticity, ie, depress pacemaker rates, especially ectopic foci rates produce moderate depression of phase 0 depolarization and thus slow conduction in atria, A-V node, His-Purkinje system, and ventricles prolong repolarization, ie, lengthen action potential duration increase refractoriness and depress excitabiHty. These electrophysiological effects are manifested in the ECG by increases in the PR, QRS, and QT intervals. 

It is an amide local anaesthetic and has rapid onset of action. It depresses diastolic depolarization and automaticity in ectopic foci in ventricular tissue. Phase 4 depolarization in partially depressed Purkinje fibres and after depolarizations are antagonised. It does not depress AV conduction and decreases action potential duration, effective refractory period. It has no effect on BP. 

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. 

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... 

This common arrhythmia involves multiple ectopic foci of atrial cells creating a chaotic movement of impulses through the atria. The ventricular response is rapid (100-150 beats per minute) and irreguiar. 

Determine cellular fate/ biodistribution and persistence (cell migration/trafficking, engraftment, differentiation, cell phenotype, fusion, tissue integration, proliferation, survival). Use of noninvasive (nonterminal) imaging modalities and special histological stains (terminal). Determine presence of ectopic foci. Justify multiple time points (e.g., 1 week, 1 month, 3 months, 6 months or 12 months). 

Cardiac arrhythmias ore caused by a disturbance in the con-duciion of the impulse through the myocardial tissue, bj disorders of impulse formation, or by a combination of ihete factors. The aniianhythmic agents used most commonly il-feet impulse conduction by altering conduction velocity aisl the duration of the refractory period of heart muscle lis iie They also depress spontaneous diastolic dcpolarizalim. causing a reduction of automaticity by ectopic foci. 

No. Decreased conduction in the AV node is not desired in this case, as the influence of the sinoatrial (SA) node is necessary to keep ectopic foci in check. 

Phase 2 of the cardiac action potential is prolonged, due to the blockade of potassium flux decreasing the excitability of tissue and thus inhibiting the spontaneous formation of ectopic foci. 

These drugs are cardiac calcium channel blockers. By decreasing calcium conduction in the calcium-dependent portions of the AV node, His bundle and in the myocardium itself, ectopic foci can be suppressed. 

Would class IV antiarrhythmics be useful in ventricular arrhythmias arising from ectopic foci in the Purkinje fibers ... 

These drugs decrease conduction in the AV node, and, thus, in therapeutic doses, mediate a partial blockade of the node. This decreases the frequency and number of ectopic foci reaching the ventricle. 

Arrhythmias arise from ectopic foci in the cardiac tissue. Recall that all cardiac myocytes have the potential for spontaneous depolarization because of their smooth muscle-like properties and the close proximity of the cell membrane to depolarization threshold. Normally, these foci are eliminated by the powerful depolarization of the SA nodal cells. Unopposed, these foci generate depolarizations that cause small premature contractions and inhibit full contraction of cardiac muscle in response to the normal SA nodal depolarization. This is of primary importance in ventricular tissue. 

Ventricular arrhythmias arise most often from cells in the bundle of His and Purkinje s fibers. These ectopic foci can cause premature contraction of ventricular cells, resulting in no beneficial... 

Multiple ectopic foci of atriai ceils generate 350-450 impulses per minute. The ventricle responds to an occasional impulse. Both atrial and ventricular rhythm are irregular. 

Erratic discharge from many ectopic foci in the ventricle. Rate is 350 - 450 beats/min. Rhythm is irregular. 

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. 

Lidocaine (e.g., Xylocaine) Depresses automaticity of ectopic foci, increases conduction velocity of A-V node and His-Purkinje. Wolff-Parkinson-White, Ventricular tachycardia. Premature vent, depolarization. Ventricular fibrillation. CNS paresthesias, drowsiness, confusion, restlessness (at low doses). At high doses, seizures or disorientation. Cardiac depression (if given by rapid IV), arrhythmias. 

Mexiletine (Mexitil) Decreases automaticity of AV node and ectopic foci. Prolongs refractory period of His-Purkinje, ventricle, and accessory pathway. Premature vent, depolarization. Ventricular tachycardia (life -threatening ventricular arrhythmias). May worsen arrhythmias, hepatotoxicity, rarely convulsions... 

Tocainide (Tonocard) Decreases automaticity of AV node and ectopic foci. Shortens refractory period in atrium, AV node, and ventricle. Prolongs refractory period in accessory pathway. (1 ff Dizziness, tremor, paresthesias, nausea, vomiting, pulmonary fibrosis, bone marrow supression. 

Automaticity is suppressed in ectopic foci by every antiarrhythmic except bretylium. 

Reduces 1) automaticity of SA node ectopic foci, 2) conduction velocity throughout. Prolongs refractory period in His-Purkinje, ventricle, and accessory pathways. 

Reduces 1) Ca++ entry into myocardial cells, 2) SA node and ectopic foci automaticity, 3) conduction and Increases refractory period of AV node. 

Not understood. A possible explanation is that because the rauwolfia alkaloids deplete the neurotransmitter from the sympathetic nerve supply to the heart, the parasympathetic vagal supply (i.e. heart slowing) has full rein. Digitalis also causes bradycardia which in the presence of the rauwolfia becomes excessive. In this situation the rate could become so slow that ectopic foci, which would normally be swamped by a faster, more normal beat, begin to fire, leading to the development of arrhythmias. Syncope could also result from the combination of bradycardia and the hypotensive effects of reserpine. 

Abstract An arrhythmia occurs as a result of abnormal electrical conduction and genesis of an abnormal electrical current. There are various types of arrhythmias that can be classified in terms of their origin as, atrial, junctional or ventricular arrhythmias. Many arrhythmias are initiated by ectopic foci. 

Can arise from either single, or multiple ectopic foci. On the ECG they can be recognised as they occur earlier than the next expected P wave and differ in morphology to the normal P waves (Fig. 6.2). Not all of these premature beats are always conducted resulting in ventricular activation and a subsequent QRS complex. This is due to the tissue being refractory and insufficiently recovered to conduct another impulse. 

Is the most commonly encountered arrhythmia. Atrial Fibrillation (AF) increases in incidence with age. It is caused by multiple electrical triggers (multiple ectopic foci) occurring in the atria (Fig. 6.20), most commonly occurring around the region of the pulmonary veins. 

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