Anti-Arrhythmic Drugs

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Class 1a Anti-Arrhythmic names

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Quinidine~~

Procainamide~~
Disopyramide

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Class 1a Anti-Arrhythmic Properties

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Na+ channel blockers
Block conduction, Increases Effective Refractory Period

Medium velocity Na+ Channels

•ClassI antiarrhythmic agents decrease abnormal automaticity of ectopic pacemakersmore than normal automaticity of SA node.

•they also decrease conduction (phase 0) and membrane responsiveness (phase 4)to a greater extend in sick rather than normal tissue.

•effects achieved by preferentially blocking Na+channels in chronically depolarized states.

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Class 1b Anti-Arrhythmic names

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Lidocaine~~

Phenytoin~~

Mexiletine

Tocainide

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Class 1b Anti-Arrhythmic Properties

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Na+ channel blockers

Block conduction, decreases Effective Refractory Period

Fast Na+ channels

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class 1c Anti-Arrhythmic names

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Encainidine

Lorceinide

Flecaininide

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class 1c Anti-Arrhythmic properties

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Na+ channel blockers

Block conduction,

No Effect on Effective Refractory Period or an Increase in Effective Refractory Period

Slow Na+ Channels

•These agentsare potent and selective inhibitors of the slow Na+ ch. associated with phase 0and thus decrease Vmax and conduction velocity.

•Approved onlyfor refractory ventricular tachycardias that does not respond to other medications

Noeffect on ventricular Action Potential Duration or QT interval; increase QRS duration;pro-arrhythmic effect.

• Encainide and flecainidesignificantly increase mortality in patients treated for arrhythmias.

Encainidine

Lorceinide

Flecaininide

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class II Anti-Arrhythmic names

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Propranolol~~

Esmolol

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class II Anti-Arrhythmic properties

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Beta Adrenoceptor Antagonist

Decrease sinus node automaticity, Sympatholythic activity

•prevent atrial arrhythmias resulting from excitation of sympathetic nervoussystem.

•Increase Effective Refractory Period of SA and AV node.

•slows ventricular rate in the presence of atrial flutter.

•slows heart rate, decrease cardiac output, and cause hypotension.

•Canexacerbate hyperreactivity inasthma.Glucose,cholesterol, CNS effects (propanolol cns activity)...

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class III Anti-Arrhythmic names

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Bretylium

Amiodarone

ibutilide

Sotadol

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class III Anti-Arrhythmic properties

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Drugs that prolong the action potential duration

No effects on conduction, delays Repolarization

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class IV Anti-Arrhythmic names

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Verapamil~~Prototype

Diltiazem Effective yet not approved for this use

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class IV Anti-Arrhythmic properties

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Ca++ Antagonist

Slows conduction velocity in the atrioventricular node

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Misc. Anti-Arrhythmic drugs names

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Adenosine~~

Digitalis

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Misc. Anti-Arrhythmic drugs

Adenosine properties

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Adenosine:

given in high doses as an IV bolus, markedlyslows conduction in the AV node.

•Probablyhyperpolarizethis tissue and reduce calcium current.•Extremely effectivein AV nodal arrhythmias and has become the drug of choice for treatment of thiscondition.

•Verylowtoxicity: includes flushing and hypotension but because its short durationof action (15 sec) these effects do not limit the use of the drug.

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Nifedipine

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NOT USEFUL AS ANTI-ARRHYTHMIC

it's effect is primarily on Vessels

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Misc. Anti-Arrhythmic drugs Digitalis

properties

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Can be useful in Tx of several forms of Arrhythmia

Not commonly used since the development of Ca++ channel blockers and Adenosine

CAN CAUSE ARRHYTHMIA!!!!

more on Digitalis in the CHF cards!

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QUINIDINE

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•Affectbothatrial and ventricular arrhythmias.

•Blocks NaCurrent and conduction velocityin atria, Purkinje fibers and ventricular cells.•Prolongs APDand ERP, and results in increased QRS and QT duration.

•antimuscariniceffects in heart and in high doses can result in excessive ventricularrate.

•OD canalso cause complete SA and AV block resulting in asystole.

•it also have alpha-adrenoreceptorblocking properties and can cause vasodilation and baroreflex-mediatedincrease in heart rate.

•Mostcommon(20%) side fx are: nausea, diarrhea, and vomiting. Can precipitate new arrhythmias(Torsade de pointes).

•Usuallyadministeredorally with 80% bound to plasma proteins (can displace digoxin), its ismetabolized in the liver and has a half-life of 6 hours.

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Procainamide

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•directcardiac effects of quinidine; sometimes used as analternative to quinidine.

•Eliminatedbythe kidney after N-acetylation, and can rise to toxic levels in renaldysfunction conditions.

•Mostcommonside effect is a hypersensitivity reaction (lupus-like syndrome)

•Closeto65% of patients will develop antinuclear antibodies with only 20% developingclinical symptoms.

•This is reversible and pts will return to normality after thedrug is stopped.

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Lidocaine

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•Blockspacemaker Na+current during phase 4 and inhibits the small inward Na+ current that normally flows duringplateau of action potential in ventricular and Purkinje cells.•Ithas minimal effects on Na+current associated with phase 0.•Reduces APD with little or no effecton ERP. (have little effects on EKG).

•Almostexclusively blocks activated/inactivatedstates of the Na+channel and therefore it has potent effects on sick cells with minimal effectson normal cells. (useful in acute ventricular arrhythmia related to ischemia)

•no interactions with ANS so it has no effect on blood pressureor any of the indirect cardiac effects associated to quinidine.

•local anesthetics, lidocaine can cause neurological side effectsincluding paresthesis,tremor, and light-headness.•metabolized by first pass effect in liver and therefore is given primarily IVwith.

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Propanolol

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Propanolol blocks the B Adrenergic Stimulation (B-adrenergicstimulation markedly increases the slope of phase 4 depolarization andtherefore increases spontaneous firing rate in SA node)

Propanolol decreases the slope by blocking B stimulation

•Class II antiarrhythmics canprevent atrial arrhythmias resulting from excitation of sympathetic nervoussystem.•Increase ERP of both SA and AV node.•Canslow ventricular rate in the presence of atrial flutter.•Canslow heart rate, decrease cardiac output, and cause hypotension.•Canexacerbate hyperreactivity inasthma.Glucose,cholesterol, CNS effects