Class IA: Antiarrhythmics 

Na+ fast channel blockers (and K+ prolongs repolarization)

"state dependent blockade" preferentially in the open or activated state

Increases AP duration and effective refractory period 

Quinidine + digoxin 

Class IA antiarrhythmic (Na+ channel blocker)

Also causes muscarinic receptor blockade which can increase HR and AV conduction (proarrhythmic)

May also cause vasodilation via alpha block w/ possible reflex tachycardia

Use: many arrhythmias but in A-fib need inital digitalization to slow AV conduction  

AE: cinchonism (GI, tinnitus, ocular dysfunction, CNS excitation), hypotension, increases QT interval assoc w/ syncope/torsades

DI: hyperkalemia (b/c drug is a weak base it can increase its absorption)

Procainamide  

Class 1A: antiarrhythmic (Na+ channel blocker)

Less muscarinic block than quinidine & NO alpha block

Metabolized via N-acetyltransferase to an active metabolite (therefore 2 active metabolites)

AE: SLE-like syndrome (more likely w/ slow acetylators), hematotoxicity (thrombocytopenia, agranulocytosis), torsades 

Class IB antiarrhythmics (lidocaine/mexiletine/tocainide)

Block fast Na+ channels ONLY

Block inactivated channels w/ preference for tissues partly depolarized (ischemic tissues) leads to less excitability for hypoxic heart muscle

Decreases AP duration leading to increased time of diastole and decreased HR

Lidocaine: local anesthetic (IV only)

Used: post MI for ventricular arrhythmias, open heart surgery, digoxin toxicity

SE: seizures, least cardiotoxic

Mexiletine/Tocainide: oral but same uses 

Class IC: antiarrhythmics

Flecainide: blocks fast Na+ channels esp. in the His-Purkinje tissue

NOT used b/c of proarrhythmogenic effects leading to increased sudden death post MI and when used in V-tach

Class II antiarrhythmics

Beta Blockers

Prevent Beta receptor activation which would normally increase cAMP

Decreases SA and AV nodal activity

Decreases Slope of phase 4 pacemaker AP

Propranolol + Acebutolol, Esmolol (last 2 are cardio selective)

Uses: prophylaxis post MI

supraventricular tachyarrhythmias

Class III: antiarrhythmics

K+ channel blockers

Delays the K+ current that allows repolarization (phase 3, increases APD & ERP)

Amiodarone

Class III: antiarrhythmic (K+ channel blocker, rectifier current which slows phase 3 repolarization) 

Mimics actually classes I, II, III, and IV

Uses: MOST effective antiarrhythmic

Binds extensively to tissues so 1/2 life = 80d

SE: Pulmonary fibrosis

Blue pigmentation of skin/thyroid dysfunction

Phototoxicity

Corneal deposits

Torsades (anything that involves the K+ channel is prone to this b/c of a genetic mutation that exists) 

Sotalol

Class III: antiarrhythmic

K+ channel blocker that slows phase 3

Beta 1 blockade which slows HR and AV conduction

Use: life threatening ventricular arrhythmias

SE: torsades

Class IV: antiarrhythmics

Slow Ca2+ channel blockers, (phase 0 & 4)

Decrease SA and AV nodal activity

Verapamil >Diltiazem (rest of CCB's end in dipines)

Uses: SVT's

SE: constipation (Verapamil), dizziness, flushing, hypotension, AV block

DI: additive AV block w/ B-blockers, digoxin

Verapamil displaces digoxin from tissue-binding site

Adenosine

unclassified antiarrhythmic

Nucleoside that activates adenosine receptors and causes a decrease in cAMP (K+ efflux & hyperpolarization)

Uses: DOC for paroxysmal SVT's (can do valsalva/carotid sinus massage) & AV nodal arrhythmias 

SE: flushing, sedation, dyspnea

Antagonized by theophylline

Magnesium

unclassified antiarrhythmic

Use: torsades (pt w/ long QT syndrome)

Drugs causing torsades: K+ channel blockers (I,III)

Antipsychotics (thioridazine)

TCA's