Kaplan Section 3 Chapter 2 Antiarrhythmic Drugs
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
|
|
||||
---|---|---|---|---|---|
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.
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Created by:
christinapham
Popular Standardized Tests sets