Antiarrhythmic drugs class I

Activity mimics all antiarrhythmic drug classes (I, II, III, and IV) blocks Na, Ca, and K channels and beta adrenoceptors. 

Local Anesthetics Binding site I S6, III S6, IV S6 Local anesthetic drugs Antiarrhythmic drugs (class I) Antiepileptic drugs Open channel inhibition... 

Drug related Use of antiarrhythmic agents (class I or class III)... 

Na+ Anticonvulsant drugs Class I antiarrhythmics Diuretic drugs Local anesthetic drugs Carbamazepine, phenytoin, valproic acid lA Disopyramide, procainamide, quinidine IB Lidocaine, mexiletine, phenytoin, tocainide IC Encainide, flecainide, propafenone Amiloride Bupivacaine, cocaine, lidocaine, mepivacaine, tetracaine... 

Quinidine is used as an antiarrhythmic agent (class I A), and it is also used rarely as an anti-malarial drug. 

Besides the class I-typical proarrhythmic risk class IA antiarrhythmics possess a marked proarrhythmic risk for the induction of torsade depointes arrhythmia (life-threatening polymorphic ventricular tachycardia observed with most action potential prolonging drugs). 

Antiarrhythmic drugs are antagonists of the fast Na+ channel, which slow the propagation of the cardiac action potential. Class I drugs suppress the fast upstroke of the action potential. 

Electrolyte disturbance Hypokalemia or hyperkalemia may alter the effects of Class I antiarrhythmic drugs. Correct preexisting hypokalemia or hyperkalemia before administration. 

Bepridil has Class I antiarrhythmic properties and, like other such drugs, can induce new arrhythmias, including ventricular tachycardia/ventricular fibrillation (VTA/F). In addition, because of its ability to prolong the QT interval, bepridil can cause torsades de pointes type VT. Because of these properties, reserve bepridil for patients in whom other antianginal agents do not offer a satisfactory effect (see Warnings). P.285... 

Dolasetron Hypersensitivity to the drug or components of the product markedly prolonged QTc or atrioventricular block II to III patients receiving class I or III antiarrhythmic agents. 

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. 

Class II antiarrhythmic drugs competitively inhibit /3-adrenoceptors and inhibit catecholamine-induced stimulation of cardiac 15-receptors. In addition, some members of the group (e.g., propranolol and acebutolol) cause electrophysiological alterations in Purkinje fibers that resemble those produced by class I antiarrhythmic drugs. The latter actions have been called membrane-stabilizing effects. 

TABLE 16.2 Cardiac Electrophysiological Effects of Class I Antiarrhythmic Drugs... 

Class I antiarrhythmic drugs are essentially sodium channel blockers.5,27,29 These drugs bind to membrane sodium channels in various excitable tissues, including myocardial cells. In cardiac tissues, class I drugs normalize the rate of sodium entry into cardiac tissues and thereby help control cardiac excitation and conduction.8,27 Certain class I agents (e.g., lidocaine) are also used as local anesthetics the way that these drugs bind to sodium channels is discussed in more detail in Chapter 12. 

Nattel S, Kneller J, Zou R, Leon LJ. Mechanisms of termination of atrial fibrillation by Class I antiarrhythmic drugs evidence from clinical, experimental, and mathematical modeling studies. J Cardiovasc Electro-physiol 2 003 14(suppl) S133—S139. 

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