Ventricular depolarization ectopic

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. 

Ventricular premature depolarizations (VPDs) are ectopic electrical impulses originating in ventricular tissue, resulting... 

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 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. 

Woosley RL, McDevitt DG, Nies AS, Smith RF, Wilkinson GR, Oates JA. Suppression of ventricular ectopic depolarizations by tocainide. Circulation 1977 56(6) 980. ... 

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. 

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... 

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