Vaughan Williams classification

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Class I: " block inward Na+ channel Class IA: (note: don t worry about the different subtypes this is not need to know) " reduce rise of action potential upstroke (phase 0)(this is known as Vmax) and prolong action potential duration " onset and offset of Na+ channel block intermediate (<5 sec) " examples: quinidine, procainamide Class IB: " shorten action potential duration, decrease rate of rise of action potential " rapid onset and offset kinetics (<500 msec) " example: lidocaine Class IC: " reduce Vmax , ie. Rate of rise of action potential (most potent effect on phase 0) " no significant effect on repolarization " minimal change in action potential duration " slow onset and offset kinetics (10 20 sec) " examples: propafenone, flecainide Class II: " beta blockers " slow sinus rate, prolong AV node conduction and refractoriness " useful in reentrant arrhythmias involving AV node, and arrhythmias triggered by stress (adrenergic stimulation) " examples: propranolol, metoprolol etc. Class III: " drugs that block K+ channels and prolong repolarization " this means an increase in duration of action potential (and QT), increase in refractoriness " examples: amiodarone, sotalol, ibutelide Class IV: " block the slow calcium channel, effect seen mostly in the sinus and AV node with decreased conduction across the AV node, and increased refractoriness " examples: verapamil, diltiazam the Vaughan Williams classification is widely known, but it has several limitations: " many of the drugs actually have actions that fit in multiple categories for example sotalol has beta blocking effects; Class IA and Class IC drugs tend to overlap in their actions; amiodarone has effects consistent with all four of the VW classes " doesn t take into account metabolites for example procainamide is metabolized to N-acetyl procainamide (NAPA) which has a class III action " this classification doesn t have a place for other drugs such as digoxin and adenosine