Antiarrhythmics II

Question 1

limitations of Vaughan Williams Classification system

Answer 1

primarily based on effects of drugs on electrophysiological characteristics of isolated, normal cardiac tissue. The classification is incomplete. Considers primary blocking effect only

Question 2

class IA antiarrhythmic drugs mechanism

Answer 2

fast (open) Na channel block. prolongs effective refractory period, prolongs action potential duration

Question 3

Quinidine, procainamide, disopyramide uses

Answer 3

secondary drug of choice for treatment of chronic Afib, PSVTs, sustained VT/VF (procainamide), acute atrial flutter/fibrillation (IV procainamide)

Question 4

Class 1A toxicities

Answer 4

QT prolongation, TdP arrhythmias, heart block, hypotension, lupus-like syndrome. GI symptoms.

Question 5

quinidine adverse effects

Answer 5

alpha adrenergic blockade -> hypotension, reflex tachycardia. M2 blockade, vagal inhibition. cinchonism, hepatitis, diarrhea, thrombocytopenia. CYP2D6 inhibition. drug interactions

Question 6

procainamide adverse effects

Answer 6

no receptor antagonism, but local anesthetic action. active metabolite NAPA leads to QT prolongation and TdP. slow acetylators lead to lupus like syndrome. IV hypotension (ganglionic block)

Question 7

disopyramide adverse effects

Answer 7

prominent anticholinergic action. heart failure.

Question 8

class IB antiarrhythmic drugs

Answer 8

Na channel block. prefers depolarized (ischemic) tissue Na channel blockade. prefers inactivated Na channels, rapidly unbinds at rest. Lidocaine, mexiletine.

Question 9

class IB clinical uses

Answer 9

secondary drug of choice for acute suppression of VT or VF. post-MI emergency VT/VF, cardioversion, digitalis toxicity. not used for atrial arrhythmias. no QT prolongation, may shorten APD slightly

Question 10

class IB toxicities

Answer 10

tremor, nausea, seizures, local anesthetic action. Lidocaine is IV only. mexiletine has GI toxicity, metabolism induced by phenytoin

Question 11

class IC drugs

Answer 11

Na channel block. slow unbinding, greatly prolongs Ina recovery which causes K channel blockaed. prolongs APD preferentially at faster heart rates. prolongs PR, QRS, QT intervals. no EADs or TdP. flecainide, propafenone, moricizine.

Question 12

Clinical uses of Class IC drugs

Answer 12

primary use for maintenance of sinus rhythm in chronic AF or SVT in patients without structural heart disease. secondary drug of choice for management of Afib, SVT. last resort drug for refractory VT.

Question 13

class IC toxicities

Answer 13

increase ventricular response to atrial flutter. contraindicated in heart failure, post MI. causes heart block.

Question 14

class II drugs

Answer 14

Beta adrenergic receptor blockers, may be nonselective or b1 selective. decreases SA, AV node activity. phase 4 depolarization. non selective: propanolol, carvedilol. b1 selective: metroprolol, acebutolol, esmolol

Question 15

clinical uses of class II drugs

Answer 15

control of ventricular rate in acute or chronic atrial flutter or fib. long term suppression of SVTs. safe and somewhat effective against PVCs. carvedilol decreases mortality in CHF.

Question 16

class II toxicities

Answer 16

heart block, bradycardia, bronchospasm, hypotension. contraindicated in WPW

Question 17

which class II is used in acute emergency?

Answer 17

esmolol. short half life.

Question 18

class III drugs

Answer 18

K channel blockade. prolongs refractoriness. major toxicity is TdP arrhythmias. sotalol, ibutilide, dofetilide, amiodarone, dronedarone

Question 19

clinical uses of class III drugs

Answer 19

maintenance of sinus rhythm in AF. long term suppression of SVT. amiodarone is primary drug of choice for VT/VF. useful against all arrhythmiaas except digitalis tox

Question 20

class III tox

Answer 20

QT prolongation, TdP, heart block, bradycardia, hypotension, bronchospasm.

Question 21

amiodarone

Answer 21

thyroxine analog. mixed actions mimics all antiarrhythmic classes. Na, Ca, K, alpha and beta adrenergic blocking effects. long half life of 80 days. causes thyroid effects, pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, corneal deposits, photosens, drug interactions. dont give with another QT prolonging drug

Question 22

dronedarone

Answer 22

less effective but fewer side effects than amiodarone

Question 23

ibutilide

Answer 23

IV for termination of atrial flutter or fib

Question 24

class IV drugs

Answer 24

L-type Ca channel blockade. Slows SA and AV node activity. prolongs AV refractoriness. Verapamil, diltiazam, nifedipine, amlodipine etc

Question 25

clinical uses of class IV

Answer 25

slow ventricular rate during atrilal flutter of AF. prevent or terminate reentrant SVTs, contraindicated in WPW.

Question 26

class IV tox

Answer 26

IV use hypotension, bradycardia, constipation, dizziness. will increase serum digoxin levels. contraindicated in WPW. AV blocking effects additive with digoxin and b blockers.

Question 27

adenosine

Answer 27

natural nucleoside. rapid IV bolus only. 10 sec half life. decreased cAMP, increase Ik,ach. decreases SA and AV node activity. terminates PSVT and AVN reentrant arrhythmias. not atrial flutter, AF, WPW, atrial tachycardia.

Question 28

magnesium

Answer 28

useful for preventing recurrent TdP and some digitalis induced arrhythmias

Question 29

cardiac glycosides/digoxin

Answer 29

Na/K pump inhibitor. positive inotropic agent for heart failure. indirect increase in Ca. vagotonic effect. slows AVN activity and conduction. low therapeutc index, may cause DAD arrhythmias

Question 30

primary treatment for acute AFib or flutter

Answer 30

rate control with IV verapamil, diltiazem, b blocker, or digoxin. DC cardioversion. precardiac surgery: b blockers, sotalol, amiodarone

Question 31

primary treatment for chronic AFib or flutter

Answer 31

rate control with verapami, diltiazem, b blocker, or digoxin. maintain sinus rhythm with amiodarone, sotalol, flecainide, propafenone, or dofetilide. radiofreq ablation

Question 32

primary treatment for acute SVTs

Answer 32

IV adenosine, verapamil, diltiazem

Question 33

primary treatment for chronic SVTs

Answer 33

b blockers, verapamil, diltiazem, flecainide, propafenone, amiodarone, sotalol, dogoxin. DC cardioversion, atrial pacing effective but rarely required

Question 34

primary treatment for PVCs or nonsustained VT

Answer 34

asymptomatic: no structural heart disease = no treatment. symptomatic: B blockers

Question 35

primary treatment for Sustained VT

Answer 35

amiodarone, ICD (intracardiac device)

Question 36

primary treatment for ventricular fibrillation

Answer 36

amiodarone, ICD

Question 37

primary treatment for cardiac glycoside-indiuced VT

Answer 37

digoxin immune fab fragments

Question 38

primary treatment for drug induced Torsades de pointes (TdP)

Answer 38

discontinue offending drug, magnesium sulfate, KCl