Biochemistry



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Phase 0


-Na channels open

-Ventricular depolarization

-Class I antiarrhythmic drugs

Phase 1

-Na channels are inactivated

-Transient outward K+ currents and inward Cl- currents contribute to the “notch”and overshoot

-No significant drug interactions

Phase 2

-Plateau phase in which slow Ca2+ influx is balanced by a late appearing K+ current.

-No significant drug interactions

Phase 3

-Repolarization phase in which delayed K+ current rapidly increases as the Ca2+ current dies out

-Class III antiarrhythmics

Phase 4

-Return of membrane to resting potential maintained by activity of a Na/K/ATP ase






ANTIARRHYTHMIC DRUGS AFFECTING THE “FAST RESPONSE” FIBERS IN THE HIS PURKINJE SYSTEM





DRUG

MECHANISM

USE

ADVERSE/COMMENTS

Quinidine


Class I

-“M” blockade

-Increased HR and AV conduction

-Blockade of fast Na+ channels

-Atrial fibrillation

-Wide clinical use

-N/V, cinchonism (GI / tinnitus / ocular dysfunction / CNS excitation)

-QT prolongation

-Drug interactions: hypokalemia enhances effects. May oppose effects of ACHe inhibitors in myasthenia

-May cause vasodilation via alpha blockade with possible reflex tachycardia

Procainamide


Class I

-Less M blockade

-No alpha blockade

-Sodium channel blockade

-Orally effective

-Atrial and ventricular dysrhythmas

-Metabolized by N acetyltransferase

-Adverse eefects include SLE type syndrome (caution in slow acetylators)

-CNS effects

-Agranulocytosis

-Torsades

Lidocaine
Class Ib


-Blocks Na channels

-Prefers action in ischemic tissues (blocks inactivated channels)

-Post MI arrhythmias

-Ventricular dysrhythmias

-Clearance dependent on liver blood flow

-Extensive first passm metabolism

-Seizures evidence of CNS toxicity

Phenytoin


Class Ib

-Na block

-Used occasionally in digitalis OD to reverse AV block

-

Flecainide / Encainide


Class Ic

-Limited use, Na channel block

-Limited

-Pro arrhythmic

-May lead to sudden death post MI

Beta Blockers


Class II

-Decrease Sa and nodal activity, decrease slop of phase 4 action potential in pacemakers (slow response currents in the SA and AV nodes)

-Prevent B1 adrenoreceptor activation

-Post MI

-Suppression of SVTs

-Esmolol in SVTs

-Hypotension

-Bradycardia

Amiodarone


Class III

-K+channel blockade

-Mimics activity of all antiarrhythmic drug classes

-Blocks Na/Ca/K channels

-Long half life

-Atrial and ventricular dysrhythmias

-Pulmonary fibrosis

-Blue pigmentation (smurf skin)
-Increases LDL-C


-Hepatic disease

-Decreases clearance of dig, phenytoin, quinidine, theophylline, and warfarin

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