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USMLE - Pharm

Kaplan Section 3 Chapter 2 Antiarrhythmic Drugs

QuestionAnswer
Class I antiarrhythmics Na+ channel blockers; slow or block conduction; used as local anesthetics
Class II antiarrhythmics B blockers
Class III antiarrhythmics K+ channel blockers; block delayed K+ rectifier current --> slows repolarization
Class IV antiarrhythmics Ca2+ channel blockers
What do Class IA antiarrhythmics do to Purkinje cells? Moderate block of fast Na channels (I-Na) --> slower depolarization --> lengthen QRS; block K+ channels (I-Kr) --> prolong repolarization; together, these increase AP duration (--> lengthen QT --> torsades de pointe) and effective refractory period.
What types of tissues do Class I antiarrhythmics prefer? State dep: damaged/ischemic tissues-->more channels in open (both M & h open) or activated state (M closed, h open)-->Na+ blockers pref act on these channels-->drugs act better on freq depolarizing tissue (tachy) or relatively depolarized at rest(hypoxia)
What would you use Class IA drugs for? Atrial fibrillation/atrial flutter
Name the drugs in Class IA. Queen Ami Proclaims that Diso's Pyramid is hers. Quinidine, Amiodarone, Procainamide, Disopyramide.
What do Class IB antiarrhythmics do to Purkinje cells? Mild block of fast Na channels (I-Na) --> slightly slows depolarization --> lengthen QRS; block slow Na+ window currents --> faster repolarization --> decrease AP duration --> increases diastole --> increases time for recovery.
What do Class IC antiarrhythmics do to Purkinje cells? Marked block of fast Na+ channels (I-Na), slower depolarization (--> increase QRS), no change in repolarization --> no change in AP duration, no effect on QT interval.
What tissues does Class IC target? His/Purkinje fibers
What do Class I (A/B/C) antiarrhythmics do to pacemaker cells? decrease the phase 4 slope (slower firing --> slows heart rate), increases the threshold for firing --> slower recovery of Na channels --> slower firing
What do Class II antiarrhythmics do to pacemaker cells? decrease the phase 4 slope (slower firing --> slows heart rate), Prolongs repolarization at AV node
What do Class II antiarrhythmics do to Purkinje cells? nothing
What do Class III antiarrhythmics do to Purkinje cells? marked prolonging of repolarization
What do Class III antiarrhythmics do to pacemaker cells? nothing
What do Class IV antiarrhythmics do to pacemaker cells? Slow rise of action potential (slower depolarization); Prolongs repolarization at AV node
What do Class IV antiarrhythmics do to pacemaker cells? nothing
Quinidine Class IA antiarrhythmic; Na+ fast channel blocker --> slows dep; K+ channel blocker --> slows repol; inc AP duration and ERP.; blocks M receptors --> inc HR and AV conduction; blocks a receptors --> vasodilation --> reflex tachy; used in atrial fibril
Side effects of Quinidine Class IA antiarrhythmic; NVD, cinchonism (ears/eyes dysfxn, GI probs, CNS excitation, vertigo/dizziness), hypotension, prolong QRS & QT --> torsades de pointe.
What drug should those on quinidine stay away from? antacids because Quinidine is a weak base and antacids will only increase Quinidine absorption --> increased Quinidine toxicity
Drug interactions of quinidine 1. enhanced by hyperkalemia 2. displaces digoxin from tissue binding sites --> more toxic 3. May oppose AchE inhibitors --> don't give to someone with myasthenia gravis!
Procainamide Class IA antiarrhythmic; Na+ fast channel blocker --> slows dep; K+ channel blocker --> slows repol; inc AP duration and ERP--> lengthen QRS and QT --> torsades; blocks M receptors (but less than quinidine) --> inc HR and AV conduction; more cardiodepress
Side effects of Procainamide 1. slow acetylators --> SLE-like syndrome 2. hematotoxicity, CNS effects (dizzy, hallucinations), lengthened QRS and QT --> torsades
Long QT Syndrome Genetic mutation in gene for K+ channels.
Which classes of drugs can increase the risk of torsades in pts with long QT syndrome? K+ channel blockers: Class III and Class IA anti-arrhythmics; Thioridazine and tricyclic antidepressants (unclassified drugs) have also been implicated in torsades.
Lidocaine Class IB antiarrhythmic; Used for Ventricular (no effect on atrial tissue) arrhythmias POST MI or arrhythmias following attempted cardioversion. Also use during open heart surg or due to digitalis poisoning.
Can you take lidocaine orally? No because of first-pass effects
What are the side effects of lidocaine OD on lidocaine --> CNS toxicity --> seizures (what Dr. Young's mom had); least cardiotoxic of the conventional anti-arrhythmics.
Mexiletine Like lidocaine, but can take orally
Tocainide Like lidocaine, but can take orally
Flecainide Class IC antiarrhythmic; can markedly slow conduction in atrial and ventricular tissue.
Encainide Class IC antiarrhythmic; can markedly slow conduction in atrial and ventricular tissue.
Side effects of Class IC anti-arrhythmics Flecainide and encainide - limited use because they have been shown to be pro-arrhythmogenic --> increased mortality post MI; only used for arrhythmias that don't respond to other drugs.
What channels does Amiodarone block? Na, Ca, K, Beta.
Side effects of amiodarone 1. microcystalline deposits in the cornea and skin -- blue pigmentation (smurf skin), 2. thyroid dysfxn, 3. tremors/paresthesias, 4. pulmonary fibrosis. 5. phototoxicity. Rarely causes new arrhythmias.
Drug-drug interactions of amiodarone interacts with everything! Decreases clearance of the following: digoxin, phenytoin, quinidine, theophylline, and warfarin.
What do Class II anti-arrhythmics do to the pacemaker action potential? Shallows out the slope of phase 4 --> prolong repolarization --> decrease SA/AV node firing --> decrease heart rate
What does B1 activation do to cAMP levels? Gs --> increase cAMP levels
What are the uses for Class II anti-arrhythmics? prophylaxis post MI; supraventricular tachyarrhythmias
What drug would you use for acute supraventricular tachyarrhythmias? IV esmolol
What do Class III anti-arrhythmics do to the action potential? Increases both AP duration as well as effective refractory period (blocks K channels)
What tissues do Class III drugs target? Purkinje and ventricular tissues
Bretylium Class III K+ channel blocker; used in life threatening ventricular arrhythmias
Side effects of bretylium releases amines and increases the relative refractory period (increased difference between AP duration and ERP) --> torsades
What does Amiodarone do to the action potential? Increases both AP duration as well as effective refractory period in all cardiac tissues, atrial and ventricular
Sotalol classified as K channel blocker; 1. blocks delayed K+ rectifier current --> dec AP duration and ERP; 2. blocks B1 --> dec AV nodal conduction --> dec HR
What is sotalol used for? prophylaxis in life threatening ventricular arrhythmias
Side effects of sotalol lassitude (dec energy); impotence; depression, torsades (K+ block), AV block (B1 block)
What are the effects of Class IV anti-arrhythmics? block Ca channels-->dec slope of pacemaker depolarization & dec phase 4 slope-->slow SA and AV nodal activity; block L-type Ca channels in cardiac tissue-->dec contractility; also in vessels-->vasodilation.
What is the prototype Class IV anti-arrhythmic? Verapamil (Ca+ channel blocker)
What are the effects of verapamil? Slows AV and SA nodal activity; also blocks vascular Ca2+ channels --> hypotension --> reflex tachycardia (like diltiazem)
When would you use verapamil and when should you avoid it? Use in re-entrant nodal and atrial tachycardias; avoid in vTach because verapamil may make it progress to vFib; also avoid if pt on B blockers.
Side effects of verapamil GI distress, dizziness, flushing, hypotension, AV block, CHF.
What are the effects of adenosine? activates a receptors --> Gi activation --> dec cAMP --> K+ OUT --> membrane HYPERpolarization --> dec SA and AV nodal activity; inc AV nodal refractory period.
When would you use adenosine? DOC for PSVT's (paroxysmal supraventricular tachy) and AV node arrhythmias
What is the half-life of adenosine? 30 seconds
Side effects of adenosine flushing, sedation, dyspnea
How do you treat torsades? 1. correct HYPO-K+; 2. correct HYPO-Mg2+, 3. stop any drugs that prolong the QT interval (those that prolong AP duration); 4. shorten AP duration with drugs such as isoproterenol or with electrical pacing
Is hyPO or hyPER K+ arrhythmogenic? Both are arrhythmogenic!
When would you use Mg2+? use as anti-arrhythmic agent in torsades
What is the mechanism of Mg2+ in anti-arrhythmic usage? interferes with the following channels: Na/K ATPase, Na, K, Ca
T or F: dihydropyridines have greater effects on the heart than verapamil and diltiazem. False. Verapamil and diltiazem have great effects on heart; possible AV block at high doses.
Nifedipine CaCB and dihydropyridine. Causes dec contractility and vasodilation. May cause reflex tachy, possible arrhythmias/MI.
Nimodipine CaCB. Used for subarachnoid hemorrhage; prevents vasospasm.
Side effect of verapamil inhibition of P-glycoprotein drug transporter
Side effects of dihydropyridines (e.g. nifedipine) gingival overgrowths and proteinuria
Amlodipine vascular-selective Ca channel blocker; used in CHF.
Created by: Missy Kratz Missy Kratz on 2008-02-05



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