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USMLE - Pharm
Kaplan Section 3 Chapter 2 Antiarrhythmic Drugs
| Question | Answer |
|---|---|
| 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:
christinapham
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